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SOME 



PHYSIOLOGICAL FACTORS 



NEUROSES OF CHILDHOOD, 



BY 

B. K. "RACHFORD, M.D. 

Professor of Physiology and Clinician to Children's Clinic, Medical Col- 
lege of Ohio; Member of Association of American Physicians 
and American Pediatric Society, etc. 




lit 5M/f / 

CINCINNATI: >7 fa ° L 

THE ROBERT CLARKE COMPANY. 

1895. 



V 



Copyright, 1895, 
By B. K. RACHFORD. 



PREFACE. 



This little book is for the most part a republica- 
tion of a series of papers first published in the 
Archives of Pediatries. 

In preparing these papers for republication I 
have thoroughly revised them and made many ad- 
ditions. The chapter on auto-intoxication has 
been entirely rewritten, so that from an unpreten- 
tious paragraph it has become the most important 
chapter in the book. 

B. K. Rachford, M.D. 

Cincinnati, Sept. 1, 1895. 

(iii) 



CONTENTS. 



CHAPTER I. 



NORMAL FUNCTIONS OF NERVE CELLS. 

Definition of term, " Neuroses of Childhood/' 1. Generation 
of nerve energy, the highest function of the nerve cell, 2. 
Amount of energy generated by a nerve cell depends on the 
degree of its functional depelopment, and on the amount of its 
healthful metabolism, 2-3. Discharge of energy, the second 
highest function of the nerve cell, 4. Nerve energy may be 
discharged automatically, 5 ; voluntarily, 6 ; or reflexly, 6. In- 
hibition of nerve energy is the third important function of the 
nerve cell, 7. Inhibition maybe voluntary, 8; involuntary, 9; 
or reflex, 9. 

CHAPTER II. 

PHYSIOLOGICAL PECULIARITIES OF THE NERVOUS SYSTEM OF IN- 
FANCY AND CHILDHOOD. 

The brain of the infant and child is morphologically and 
functionally immature, 11. Throughout infancy and childhood 
it develops slowly in weight and structure, and much more 
slowly in function, 12-13. Feeble inhibition of nerve energy 
is an important peculiarity of the nervous system of infancy 
and childhood, 15. Unfavorable conditions of food, heredity, 
and environment, may produce abnormally feeble inhibition, 
16-20. Lack of sensitiveness of the motor areas in infants pro- 
tects against reflex neuroses, 21 ; and produces lack of tone in 
the sphincter muscles of the young infant, 21-23 

(v) 



VI CONTENTS. 



CHAPTER III. 

FEVER AND THE VARIABLE TEMPERATURES OF CHILDHOOD. 

Definition of fever and high temperature, 24-25; of thermo- 
genic and thermo-inhibitory heat centers, 26. Thermogenic 
centers are at base of brain, 27. Thermo-inhibitory centers 
are in cerebral cortex, 27. Destruction and irritation of heat 
centers influence body temperature, 27-28. Thermogenic cen- 
ters are functionally mature at birth, 29. Thermo-inhibitory 
centers are immature at birth, 30. Immaturity of inhibitory 
centers is responsible for the variable temperatures of infancy 
and childhood, 31-34. Bacterial products, are the most import- 
ant of the exciting causes of fever, 35-37. Other exciting 
causes of fever are insolation, 38; muscular action, 38; and 
mechanical and reflex causes, 40. 



CHAPTER IV. 

HEAT DISSIPATING MECHANISM. 

We keep ourselves cool by radiation of heat from surface of 
the body, 42-43 ; by evaporation of water from the surface of 
the body. 43 ; and by evaporation of water from the air passages, 
44. Loss of heat from the surface of body is three-fold greater 
in the infant than in the adult, 43. Polypncea may, in the in- 
fant, be a means of reducing high temperatures, and may be 
therefore a symptom of fever, 45-46. 

CHAPTER V. 

AUTOGENETIC AND BACTERIAL TOXINES. 

Auto-intoxication is self-poisoning, 48. Bouchard says that 
normal urine contains seven toxic substances, 49. It is path- 
ological rather than normal urine that holds the secrets of 
auto-intoxication, 52. Uric acid and urea are not poisonous, 52- 
55 ; and are therefore not the cause of the nervous symptoms 
of the uric acid diathesis, 55. Paraxanthin and xanthin are 



CONTENTS. Vll 

poisonous leukoinains, present in the blood during attacks of 
migraine and kindred nervous disorders, 57. Leukomain 
poisoning is due to these and other unnamed poisonous leu- 
komains, 57. It is a factor in the etiology of leukomain epilepsy, 
60 ; true migraine, 62 ; leukomain gastric neurosis, 63 ; neuras- 
thenia, 65 ; hypochondriasis, 65 ; uremia, 62 ; gout, 65 ; and lead 
colic, 65. Biliary toxemia is not an unimportant form of auto- 
intoxication, 65. Bacterial toxemia is an important factor of 
the neuroses of childhood, 66. It is in part responsible for the 
nervous symptoms of the acute infections, 67 ; for the tubercu- 
lous neuroses of childhood, 68 ; for the malarial neuroses, 69 ; 
and for the neuroses associated with acute and chronic intes- 
tinal fermentation, 70. 

CHAPTER VI. 

VENOUS CONDITION OP THE BLOOD. 

Arterial anemia and venous congestion of nerve centers 
produce same symptoms, 73-74. t Motor centers of cord made 
excitable by anemia, 75-76 ; and venous congestion, 76-77. 
Weak heart produces nervous symptoms by feeble capillary 
circulation, 78. 

CHAPTER VII. 

AN IMPOVERISHED CONDITION OF THE BLOOD. 

Innutrition of nerve elements results from thin blood, 81. 
It is not an important factor of neurotic disease in children, 82- 
83. Malnutrition of nerve elements results from bad blood, 85. 
It is an important factor of neurotic disease in children, 85-92. 
The most important forms of malnutrition result from chronic 
anemia, 85 ; proteid and oxygen starvation, 86 ; fat starvation, 
87 ; and calcium starvation, 88. 

CHAPTER VIII. 

REFLEX IRRITATION. 

Reflex irritation is one of the most important factors of neu- 
rotic disease in children, 92. It acts conjointly with other 
factors, 94. Overwork produces changes in the nerve cell 7 



Vlll CONTENTS. 

95-99. Peripheral irritation produces changes in the nerve 
cell, 98-99 ; and an increased excitability of the cell thus ir- 
ritated, 98-100. The cell recovers slowly from overwork or 
prolonged irritation, 98-99. This explains the slow recovery 
of spinal irritability after the reflex cause has been removed, 
100-101 ; and gives to reflex irritation great importance as a 
factor of neurotic disease, 101-103. 

CHAPTER IX. 

EXCESSIVE NERVE ACTIVITY. 

Excessive brain work and nerve excitement are important 
factors of neurotic disease in delicate children, 106-114. Child 
is not a little man, 108. Porter demonstrated a physical basis 
for precocity in school children, 108-109. This is due to disease 
and bad heredity, 110-111. Heredity or acquired nervous 
weakness may be developed into actual disease, 113. Early 
precocity is an abnormal condition in the human infant, 113. 
Solitude in childhood gives independence of thought and 
character to the future man, 115. Play-grounds for children 
are greatly needed in all our large cities, 116-117. 



SOME PHYSIOLOGICAL FACTORS 



NEUROSES OF CHILDHOOD. 



NORMAL FUNCTIONS OF NERVE CELLS. 

The term " Neuroses of Childhood" is here used 
to cover all local and general nervous disorders 
which do not depend on known local pathological 
lesions of the nervous system. This definition of 
the term neuroses does not imply that these diseases 
have an entirely unknown pathology, but only that 
they can not be morphologically classified. In 
these diseases we know more of the symptoms than 
we do of the lesions, more of the effect than we do 
of the cause, more about the disordered functions 
of nerve cells than we do of the widely vary- 
ing pathological conditions which produce these 
disordered functions, and this is the reason why 
these diseases are incorrectly called functional 

nervous diseases. 

(1) 






2 Rachford : Neuroses of Childhood. 

The first requisite to the study of the abnormal 
functions of nerve cells should be a knowledge of 
the normal functions of nerve cells. For this 
reason the following preliminary physiological out- 
line is introduced. 

Nerve cells have three important functions, viz.: 
to generate, to discharge and to inhibit energy. 

The highest function of the nerve cell is to gen- 
erate energy. By this is meant that the cell trans- 
forms and appropriates existing energy. The amount 
of existing energy is constant, the cell does not and 
can not originate energy, but in the chemical meta- 
bolism necessary to the life of the cell force is de- 
veloped which is transformed into^ that form of 
nerve energy which is the special function of the 
individual cell (Prof. J. Gad — personal communica- 
tion), and this nerve energy is stored up to be dis- 
charged in the exercise of the cell's peculiar func- 
tion. From this it would follow that the generation 
of nerve force would be directly dependent on the 
healthful chemical metabolism ot the nerve cell, 
but it does not follow that the amount of energy 
thus developed would always be commensurable 
with the physical waste or the chemical metabolism 
going on in the cell. This disproportion between 
cell activity and the amount of force developed is 



Rachford : . Neuroses of Childhood. 3 

especially noticeable in the immature nerve cells of 
the child. A most marked example of the slight 
amount of energy developed by the cell activity of 
immature cells may be noted in cortical cells of the 
brain of the infant, and the brain of the unintel- 
ligent adult. In such brains the cortical cells con- 
cerned in the development of mental energy have 
going on within them an active chemical metabol- 
ism with the development of very little mental 
energy, and this failure of chemical metabolism to 
develop commensurate mental energy is due to the 
incomplete functional development of these cells. 
Of all the cells in the body the cell that develops 
mental energy is the slowest in reaching the degree 
of functional perfection for which it is destined, 
and it only does so after a judicious training in the 
exercise of its peculiar function throughout a 
long period of about twenty-three years. 

The functional development of the motor cell is 
much more rapid, and the disproportion between 
the amount of cell activity and force produced is 
not so great as in the mental cell, but nevertheless 
it may be stated as a fact true for all nerve cells 
that the amount of energy w^hich a cell is capable 
of generating will depend on the degree of func- 
tional development which the cell has attained. 



4 Rachford : Neuroses of Childhood. 

But these facts concerning the difference in the 
amount of cell energy developed by different cells 
under the same conditions do not in any way 
modify the force of the statement made above that 
nerve energy is directly dependent on the chemical 
metabolism of the nerve cell. It will therefore be 
permissible for us to say that other conditions be- 
ing the same, the amount of energy developed by a 
nerve cell will directly depend on the amount of health- 
ful chemical metabolism going on within it. This 
point in the physiology of the development of cell 
energy is very important, since upon it rests the 
conclusion that insufficient nourishment will dimin- 
ish the capacity of the nerve cell for the generation 
of energy. The maximum amount of energy will 
therefore be found stored in the well nourished cell, 
and the minimum amount of energy in the starved 
cell. We shall see later that this statement which 
has important clinical bearing can be strongly sup- 
ported by experimental evidence. 

Discharge of nerve energy is a function of the 
nerve cell only second in importance to the generation 
of energy. The more or less constant discharge of 
force is an automatic function of the nerve cell, and 
this unconscious discharge of nerve impulse is the 
regulating function that controls the whole body 



Rachford : Neuroses of Childhood. 5 

mechanism. As an example of this automatic dis- 
charge of nerve force one may cite the influence of 
the central nervous system over involuntary mus- 
cular tissue, whereby the " muscular tone " of in- 
voluntary muscles is maintained, the vaso-motor 
center in the medulla oblongata has such an in- 
fluence on the muscular coats of blood-vessels as to 
keep them in a state of normal contraction best 
adapted for the purposes which they serve, this 
vascular tone remains much the same at all times 
except when the functions of the center are per- 
verted by some change in the metabolism of the 
cells or by influences acting on the center either 
directly or in a reflex manner. But possibly of 
even greater importance to us in this study is the 
tonic influence of the spinal motor cells on the 
sphincter muscles of the stomach, the anus and 
the bladder, all of which are dependent on the 
spinal cord for their normal muscular tone. The 
" muscular tone " of these sphincter muscles is 
easily disturbed by reflex stimulation, producing 
on the one hand spasmodic stricture and on the 
other incontinence. The muscular tone of the 
skeletal muscles is likewise said to be maintained 
by an automatic discharge of nerve force, and a 
perversion of this function may in the same man- 



6 Kachford : Neuroses of Childhood. 

ner produce complete relaxation or irregular spas- 
modic contraction of these muscles. These ex- 
amples on the part of the muscles are sufficient to 
illustrate how nerve cells, by the automatic dis- 
charge of nerve force regulate the whole body 
mechanism. It would be of no value for us to dis- 
cuss whether this more or less constant discharge 
of nerve force is purely an automatic function 
of the cell or whether it is due to unconscious 
afferent impulses producing a reflex discharge of 
force. It is sufficient for us to know that these 
phenomena exist and it is a matter of words 
whether we speak of them as automatic or as 
reflex. 

Nerve force may also be discharged voluntarily. 
This power of willing the discharge of nerve im- 
pulses resides in the cortical cells of the cerebrum. 
The influence of the will over the discharge of 
force, by the spinal motor cells, is a physiological 
fact of great clinical importance in the study of the 
neuroses of childhood. 

Thirdly and lastly and most important of all, so 
far as our present Btudy is concerned, nerve force 
may be discharged reflexly ; this reflex discharge of 
force occurs when nerve cells are acted on by out- 
side stimuli. If the stimulus be mild the reflex 



Rachford : Neuroses of Childhood 7 

discharge of energy from the normal motor cells 
of the cord occurs only through the paths of least 
resistance, viz.: the afferent nerves in the same 
plane and on the same side as the nerve fiber that 
carried the afferent stimulus, but if the stimulus be 
more severe the reflex discharge of force will also 
occur in the same plane but on both sides of the 
cord. We shall see later how these simple laws of 
reflex action have little control over the reflex dis- 
charge of nerve force under certain pathological 
conditions. 

Inhibition of nerve energy is the third important 
function of the nerve cell. Certain cells through- 
out the central nervous system have the power of 
inhibiting energy discharged by other cells and it 
is also possible that some cells of high functional 
development may have the power of inhibiting 
their own energy. But however this may be it is a 
well established fact that inhibition does exist and 
that this power of inhibiting nerve energy may be 
either voluntary or involuntary. Voluntary inhi- 
bition of mental and motor force is a function pe- 
culiar to the cells of the cerebral cortex, but invol- 
untary inhibition of nerve force is a function of 
cells every-where distributed throughout the cen- 
tral nervous system, but the higher centers are 



8 Rachford : Neuroses of Childhood. 

always the predominating centers when the nerv- 
ous system is intact. The spinal cord contains 
cells or collections of cells (centers), which are ca- 
pable of being excited reflexly so as to give motor 
expression to sensory stimulation, and inhibition 
can best be understood by studying the inhibitory 
influence of the higher centers on spinal reflex acts. 
The spinal reflex centers can act quite independ- 
ently of higher centers. Gad demonstrated that 
after section of the spinal cord at any point, the 
centers below the section are still active and capa- 
ble of translating sensory impressions into motor 
acts. But this absolute autonomy of the spinal re- 
flex centers does not exist when the spinal cord is 
in normal communication with the brain, then the 
reflex centers in the cord are more or less under 
control of other centers higher up in the cord, the 
medulla oblongata and the brain. These centers 
may influence the lower spinal centers not only in 
causing them to discharge force as we have above 
noted but also in inhibiting their reflex acts which 
are discharged from any cause whatsoever. Some 
of the inhibitory influences coining from the brain 
are voluntary and probably originate in the cells of 
the cerebral cortex, for example we can by vol- 
untary inhibition control the urinary bladder re- 



Rachford : Neuroses of Childhood. 9 

flexes and prevent urination even when the mictu- 
rition center in the lumbar cord is strongly stimu- 
lated, and again there are spinal reflexes over 
which voluntary inhibition has no control, as for 
example erection, ejaculation, and movements of 
the iris. 

Of even more importance to us in the study of 
the neuroses of childhood are the involuntary in- 
hibitory centers which are distributed throughout 
the central nervous system. They are found in the 
brain, the medulla oblongata, and the spinal cord; 
and without voluntary effort or apparent reflex 
stimulation these centers seem to exert a constant 
inhibitory influence on the lower spinal centers. 
Setchenow's inhibitory center in the medulla ob- 
longata is an example of similar centers which we 
have reason to believe exist in the large ganglia at 
the base of the brain. The inhibitory influence of 
this center on spinal reflex acts has been quite sat- 
isfactorily demonstrated. It is also easy to demon- 
strate in a brainless frog that stimulation of the sci- 
atic nerve will inhibit spinal reflex acts. It is clear 
therefore that spinal inhibition may be brought 
about by other impulses than those that come from 
predominating centers in the brain and medulla 
oblongata, that is to say by impulses which are not 



10 Ivachford : Neuroses of Childhood. 

in themselves of a specifically inhibitory nature, but 
originate in the peripheral stimulation of sensory 
nerves. But it is not necessary for me to narrate 
experiments bearing on the subject of inhibition of 
nerve force, for such experiments are so satisfac- 
torily detailed in the physiologies that I need here 
only say that experimental physiology teaches us 
to believe that there are cells every-where distrib- 
uted throughout the central nervous system, which 
have' the power of inhibiting nervous energy. It 
matters little to us in the present study, whether 
this inhibition is always the special function of cer- 
tain cells or whether it may also be the function of 
the nucleus of the cell that discharges the energy ; 
but it is important for us to know that inhibition 
exists both for mental and motor acts, and it will 
appear later why a clear understanding, of the in- 
fluences that control and disturb inhibition is of the 
utmost importance to us in the study of the neu- 
roses of childhood. If kept in mind, the above 
outline of the normal functions of the mature 
nerve cell will materially assist in the study of the 
functional peculiarities which are manifested by the 
immature cells of the rapidly developing nervous 
system of the child. 



Rachford : Neuroses of Childhood, 11 



II. 



PHYSIOLOGICAL PECULIARITIES OF THE NERVOUS SYSTEM 
OF INFANCY AND CHILDHOOD. 

If we turn, to our text-books on physiology or 
diseases of children to inquire into the peculiarities 
of the nervous system of infancy and childhood, we 
shall close them with the feeling that very little is 
known of this important subject. While unfor- 
tunately this conclusion is for the most part true, 
yet we are not so wholly devoid of knowledge on 
this subject as our text-books might lead us to 
infer. We have at least some knowledge of a few 
of the physiological peculiarities of the immature 
nervous system of the child that have a most im- 
portant etiological import in the study of the neu- 
roses of childhood, and it is my purpose here to 
outline such of these peculiarities as I believe to 
have a bearing on neurotic disease. At birth the 
brain is morphologically and functionally the most 
immature of all the great organs of the body. 
From birth up to seven years of age it develops 
enormously in weight, in structure, and in func- 



12 Rachford : Neuroses of Childhood. 

tion. At this time the brain has attained ninety 
per cent of its maximum weight (Boyd), and after 
this slowly increases in weight up to the age of 
eighteen, but increase of function does not keep 
pace with increase of weight, the brain of a child 
of eight is almost as large as the brain of an adult, 
but as Clouston aptly says, " the difference between 
what the brain of a child of eight and the brain of 
a man of twenty-five can do and can resist is quite 
indescribable. The organ at these two periods 
might belong to two different species of animals so 
far as its essential qualities go." While the rapid 
increase in weight of the brain does not continue 
after the seventh year, the rapid increase in the 
brain's functional development goes on and still 
continues long after the brain at eighteen has 
reached its maximum weight. Clouston says " the 
unique fact about the nerve cell is the extreme 
slowness with which it develops function after its 
full bulk has been attained. * * In this it differs 
from any and every other tissue. * * We may say 
that after most of the nerve cells of the brain have 
attained their proper shape and full size, it takes 
them the enormous time of eighteen or nineteen 
years to attain snch functional perfection as they 
are to arrive at." It is an important fact that 



Rachford : Neuroses of Childhood. 13 

should always be kept in mind that the entire ner- 
vous system of the normal infant and child is con- 
stantly undergoing structural and functional de- 
velopment, and that the structural development, so 
far as we are now able to judge by our instruments 
of precision, is much more rapid than is the de- 
velopment of function. It is also a fact that even 
with normal children, this development of structure 
and function does not always go on with the same 
rapidity, nor does it always follow a regular order 
in its development. It is quite within the limits 
of health that certain functions may be rapidly de- 
veloped and that other functions may be unusually 
retarded in development. The innumerable con- 
ditions of heredity and environment have their in- 
fluence on the nervous system of the child in de- 
veloping and retarding both structure and function, 
and this interference with the order of development 
is not an abnormal condition if within a reasonable 
time the delayed functions reach a normal state of 
development. But it is not my purpose to enter 
deeply into this phase of my subject. I only wish 
here to call attention to the following important 
facts : 

1st. At birth the nervous system is structurally 
out more especially functionally immature. 



14 Rachford : Neuroses of Childhood. 

2d. Throughout infancy and the earlier years of 
childhood the brain normally undergoes rapid 
structural development. 

3d. Throughout the entire period of infancy and 
childhood the brain normally undergoes rapid func- 
tional development. 

4th. Innumerable conditions of heredity and en- 
vironment have much to do with the rapidity and 
the order of development of the functions of the 
nervous system of the normal child, as well as with 
the failure and retardation of their development in 
the abnormal child. 

5th. The metabolism in the normal immature 
nerve cell of the child must be rapid enough not 
only to supply the functional waste, but also to 
supply the material for the growth and develop- 
ment of cells. 

6th. The structural instability of the functionally 
weak and immature nerve cell of the child makes 
it much more irritable and excitable than the stable 
mature nerve cell of the adult. 

With these general considerations of some of the 
functional peculiarities of the nervous system of 
childhood, let us pass to the consideration of cer- 
tain special functions of the nervous system, which 
are not the same in childhood as in adult life. 



Rachford : Neuroses of Childhood, 15 

The feeble inhibition of nerve energy is from a 
clinical stand-point the most important physiological 
peculiarity of the nervous system of infancy and 
childhood. The inhibitory function of the nerve 
cell is the last to be developed ; the cell first ac- 
quires the function of generating energy, then the 
function of discharging energy, and lastly the func- 
tion of inhibiting or co-ordinating energy. These 
functions of the cell are developed in the order in 
which they are needed. Until energy is generated 
there can be no occasion for a discharging function, 
and until energy is discharged there can be no oc- 
casion for an inhibiting function. Feeble inhibition 
is therefore one of the physiological characteristics 
of the immature nervous system of infancy and 
childhood, and it plays a most important role 
as a predisposing factor of the neuroses of child- 
hood. Otto Soltsman noted that inhibition was 
very feeble in young animals, and that it be- 
came stronger as the animal got older. The inhib- 
itory function of cells is therefore in this regard 
like the generating function, it gradually becomes 
stronger as the cells get older up to the time when 
they reach their complete functional development. 
But it must be remembered that the inhibitory 
function of a cell is always developed later than 



16 Rachford : Neuroses of Childhood. 

that function of the cell which generates the force 
which is to be inhibited. In the normal order of 
things the function of inhibition should closely fol- 
low the development of the function which gener- 
ates the force to be inhibited. 

The inhibitory mechanisms which control the 
discharge of nerve force that regulates such vital 
processes as the action of the heart and the lungs 
are fairly well developed at birth, while those that 
regulate reflex phenomena are slowly developed 
during infancy and early childhood, and voluntary 
inhibition of motor and mental force does not find 
its complete development till long after childhood 
has passed. The late development of the function 
of inhibition is a fact of prime importance from a 
clinical stand-point, because this is the last function 
of the cell to develop and is the one that is most 
likely to be still further retarded in development 
by unfavorable conditions of heredity and environ- 
ment. It is therefore the abnormally feeble inhibition 
which occurs in the abnormal child that is such a potent 
factor in the production of neurotic disease in infancy 
and childhood. It is my belief that this functional 
immaturity of the inhibitory centers is most im- 
portant in explaining the manner in which child- 
hood acts as a predisposing cause of such reflex 



Bachford : Neuroses of Childhood. 17 

neuroses as convulsions and incontinence of urine. 
It is evident that this cause, most potent at birth, 
gradually grows less as the child grows older. This 
is especially true of voluntary inhibition. At birth 
voluntary inhibition, if it exists at all, must be 
very feeble, and it gradually grows stronger as the 
higher functions of the brain are more and more 
developed. We have a good example of voluntary 
inhibition in the influence of the will over urina- 
tion. One wills to urinate and the impulse passes 
down the cord to the lumbar center that presides 
over urination, and it is there translated into the 
reflex act of micturition, or on the other hand one 
wills not to urinate and the impulse travels down 
the cord to the lumbar center, and the act of urina- 
tion is inhibited. 

But the functional immaturity of the involuntary 
centers is of even more importance to us as clini- 
cians than the voluntary, for these centers have 
most to do with co-ordinating and regulating spinal 
reflex movements, the lack of inhibition on the 
part of these centers would make it possible for an 
overflow of spinal reflex movements to occur and 
in this way predispose to such convulsive disorders 
as eclampsia, chorea and epilepsy. As previously 
noted the reflex discharge of energy from the 



18 Rachford : Neuroses of Childhood. 

spinal motor cells occurs normally through the 
paths of least resistance, that is in the same plane 
and on the same side, or in the same plane and on 
the opposite side of the cord from where the nerve 
fiber entered that carried the afferent stimulus. 
But if the resistance to the spreading of the reflexes 
up and down the cord be reduced, or if the excit- 
ing stimulus be increased, then we may have an 
overflow of energy up and down the cord exciting 
general spinal reflex movements. As above stated, 
these spinal reflex movements are inhibited and an 
" overflow" of energy prevented by the action of 
involuntary inhibitory centers higher up in the 
cord, the medulla oblongata and the brain. The 
normally feeble inhibition of infancy predisposes to 
such an " overflow " of spinal reflexes, or, in other 
words, to convulsive disorders of all muscles ope- 
rated through spinal motor nerves. It is also easy 
to understand how unfavorable circumstances of 
environment and heredity, having their greatest re- 
tarding influence on the development of the in- 
hibitory function of the immature nerve cells of the 
infant and child, would still further predispose to 
overflow of spinal reflexes and in this way to con- 
vulsive disorders. By this overflow of nerve energy 
we may have a large number of spinal reflex move- 



Rachford : Neuroses of Childhood. 19 

merits as the result of a single exciting stimulus. 
Extensive convulsive movements of almost the en- 
tire body may in this way be caused by some sim- 
ple discharging stimulus. It is one of the functions 
of the reflex inhibiting mechanisms to prevent this 
overflow, so that an impulse sent to one portion of 
the cord may not overflow and spread to other por- 
tions of the cord, but the mechanism being ineffi- 
cient the inco-ordinated and spasmodic muscular 
movements occur. This overflow of nerve force is 
not peculiar to spinal cells exhibiting motor energy, 
but it also occurs in the cortical cells exhibiting 
mental energy (insanity). Inhibition against this 
overflow is quite as important in the brain cortex 
as in the spinal cord. 

It is of clinical importance that we should here 
note that, not only are the reflex centers in the gray 
or sensory portion of the cord, but the conducting 
fibers by which reflex movements overflow and 
spread up or down the cord are also in the sensory 
tract of the cord, for this gives us a partial ex- 
planation of how certain drugs such as cimicifuga, 
the bromides, antipyrin, and gelsemium, by de- 
pressing the sensory tracts of the cord can control 
reflex spinal movements. But it must be remem- 
bered that these drugs given in this way are given 



20 Rachford : Neuroses of Childhood. 

to relieve symptoms and do not have a curative in- 
fluence by removing the cause of the disease. In 
this connection I may quote Lauder Brun.ton, who 
says that " spasm is as a rule due to diminished 
action of the co-ordinating or inhibitory centers, 
rather than to excess of action in the motor cen- 
ters/' and " those drugs which stimulate the circu- 
lation and increase the nutrition of the higher nerve 
centers and the co-ordinating power tend to pre- 
vent spasm." In this we have an explanation of 
the benefit derived from nitro -glycerine in certain 
nervous conditions where the circulation is feeble 
and the malnutrition great. 

In the light of the influence of feeble inhibition 
as a factor in the production of spasm and other 
neuroses, one notorious fact demands explanation, 
and that is that the first half year of life, when in- 
hibition is most feeble, convulsive disorders are 
least frequent. There are a number of reasons why 
this is so. The most important is that the motor 
areas of newly born animals are not so sensitive 
and do not so readily respond to reflex or direct 
irritation as in older animals. Another reason is 
that the nervous system of the nursing child is not 
so frequently excited by reflex or direct irritants as 
the child that is fed on a mixed diet. 



Rachford : Neuroses of Childhood, 21 

Lack of sensitiveness of the motor areas in in- 
fants has an important bearing on the study of reflex 
neuroses. The motor areas of the nervous system 
of the newly born do not respond to electrical or 
other stimuli as readily as in older animals. Purely 
reflex neuroses are therefore very uncommon in the 
very young infant. There is at this time in life 
very little need for the inhibitory control of spinal 
reflex acts by higher nerve centers, because the 
spinal reflex centers are so functionally immature 
that we get but a minimum reflex from a maximum 
excitation. The feeble inhibition of early infancy 
is for this reason* not so potent a factor in produc- 
ing disease as it is a little later on, when inhibition 
is found not to have kept pace with the develop- 
ment of cell excitability. The reflex centers very 
early in life take on their normal irritability while 
the inhibitory function is very slow in reaching 
fall development. In this way feeble inhibition 
comes to play an important role in the production 
of the neuroses of childhood. This lack of sensi- 
tiveness of motor centers in the young infant has 
yet another important bearing, since it is in great 
part responsible for the lack of tone of the sphincter 
muscles of the infant. 

I have previously noted that the muscular tone 



22 Rachfokd : Neuroses of Childhood. 

of the sphincters was maintained by an automatic 
function of the central nervous system, so closely 
analogous to reflex action that it seems a difference 
of name rather than of function. Now these reflex 
or automatic functions of the cord are so immature 
in the newly born that there is a lack of tone of all 
sphincter muscles, that is to say an absence of the 
normal amount of contraction which afterward fits 
them for the purposes they are to serve, and which 
depends in great part upon the action of normal 
reflex centers in the cord. This lack of sensitive- 
ness of the reflex centers of the cord in the infant 
is in my opinion, a most important'factor in produc- 
ing the incontinence which is characteristic of in- 
fantile sphincters. The incontinence of infantile 
sphincters passes away with the functional develop- 
ment of the centers whose function it is to main- 
tain in them the normal amount of muscular tone 
that fits them for the purposes they are to serve. 
Abnormal conditions of heredity and environment 
may much delay the functional development of 
these centers and for this reason a complete or par- 
tial incontinence may continue long after the pe- 
riod when it should normally disappear. During 
this period, when involuntary inhibition is so 
feeble, voluntary inhibition is of great service in 



Rachford : Neuroses of Childhood. 23 

preventing, as it usually does, the diurnal inconti- 
nence. But at night when the will is asleep a 
minimum reflex will overcome the feeble involun- 
tary inhibition and cause a relaxation of the 
sphincters. Besides this any abnormal conditions 
of heredity or environment which increase the irri- 
tability of these reflex centers will also make it 
possible for slight reflex causes to disturb the 
"muscular tone" of sphincters and cause either 
spasmodic stricture or incontinence. The patho- 
logical conditions therefore which produce feeble 
inhibition and excitable nerve centers are sufficient 
explanation, for the not infrequent condition of in- 
continence of sphincters during childhood, and it 
is not necessary to invoke a cause which does not 
as a rule exist, viz., insufficient muscular develop- 
ment. 



24 Rachford : Neuroses of Childhood. 



III. 



FEVER AND THE VARIABLE TEMPERATURES OF CHILD- 
HOOD. 

It is a well-known fact that children are more 
prone to fever than adults, and it is also well 
known that the temperature is more variable in the 
fevers of infancy and childhood than it is in the 
fevers of adults. Why this is so, is a question 
which we now wish to study from a physiologic 
stand-point. But first let us clearly understand what 
we mean by the terms high temperature and fever. 

By high temperature is meant an increase of the 
body heat, whether it be due to increased heat pro- 
duction or diminished heat dissipation. When 
high temperature is due to increased heat produc- 
tion it is a symptom of fever, but when it is due to 
diminished heat dissipation it is not a symptom of 
fever. 

By fever is meant an abnormal increase of those 
tissue changes by which the normal heat of the 
body is produced, that is to say an abnormal in- 
crease of the chemic changes which result in disor- 
ganizing tissues and breaking them up into car- 



Rachford : Neuroses of Childhood. 25 

bonic acid, water, urea and other products of retro- 
grade metamorphosis. 

The fever process is characterized by a chain of 
symptoms with which every clinician is familiar, 
the most characteristic of these symptoms is in- 
crease of body temperature. But it must be re- 
membered that the height of the body temperature 
does not always mark the severity of the fever pro- 
cess, and that even a severe and wasting fever may 
exist with a subnormal temperature. One may 
note at least two reasons why the temperature is 
not an index of the severity of the fever process. 
First : increased heat production is but one of the 
symptoms of fever, which is ordinarily but not nec- 
essarily produced by the same causes that produce 
fever. Second : even should heat production keep 
pace with the severity of the fever process, heat 
dissipation may be so rapid or so variable that the 
body heat at any given time would not be an index 
of the fever process. With this understanding, the 
terms fever and temperature will be used as above 
defined, and we can proceed to study the influence 
of the nervous system on these processes. 

Increased tissue metabolism, which is the one 
great cause of increased heat production (fever), is 
under the direct control of the nervous system, and 



26 Rachford: Neuroses of Childhood, 

the centers which control this metabolism and in- 
directly the production of body heat are called heat 
centers.* Certain of these heat centers have the 
function of discharging force which will increase tis- 
sue metabolism and thereby increase the body heat, 
they are for this reason called thermogenic centers. 

Other so-called heat centers have the power of 
inhibiting or controlling the discharge of force 
from the thermogenic centers, and they are for 
this reason called ther mo -inhibitory centers. These 
thermo-inhibitory centers have no direct influence 
over the processes whereby the body heat is pro- 
duced ; yet they are of the greatest clinical impor- 
tance because of their control over the thermogenic 
centers. 

The thermogenic and thermo-inhibitory centers 
have their functions so nicely balanced in the nor- 
mal adult nervous mechanism that, with the aid of 
the heat-dissipating centers, they are able to main- 
tain the body at almost an uniform temperature 
under the most adverse circumstances, and this 
temperature equilibrium can only be disturbed by 
some maladjustment of this nervous mechanism, 
which would produce either increase or decrease of 
the body temperature. 

* Metabolism centers might be a better name for these 
centers. 



Rachford : Neuroses of Childhood. 27 

Where are these heat centers located ? Ott, 
Richet, Sachs, Aronson, Wood, Reichert, Girard, Ba- 
ginski and White agree that the dominating thermo- 
genic or heat producing centers are situated at the 
base of the brain in or near the corpus striatum. 
Eulenberg, Landois, Wood, Ott, Reichert and 
White agree that important thermo-inhibitory cen- 
ters are located in the cerebral cortex, and they are 
known as the cruciate and Sylvian centers. 

As a prelude to the use of these physiologic data 
in the explanation of some important clinical phe- 
nomena associated with the diseases of infancy and 
childhood, let us first inquire, what should one ex- 
pect, in the light of these facts, would be the influ- 
ence on the body temperature of disease or injury 
of the parts of the brain containing these centers? 

1st. Destruction of that portion of the cerebral cor- 
tex containing the cruciate or Sylvian inhibitory 
heat centers should cause a rise of temperature be- 
cause the inhibitory influence of these centers on 
the basal thermogenic centers would be wholly or 
partially withdrawn. Experimental physiology 
confirms this deduction. This is probably the ex- 
planation of the fever that follows cerebral haem- 
orrhage into the cortex, and a partial explanation 
of the fever of insolation. 



28 Rachford : Neuroses of Childhood. 

2d. Irritation of these cortical inhibitory centers 
should cause a sub-normal temperature by strength- 
ening the inhibitory control which they exercise 
over the thermogenic centers ; this is also evidenced 
by physiologic experiments. We have here an ex- 
planation of the sub-normal temperature which 
may result from cortical meningitis and from 
haemorrhage, foreign bodies or depressed bone, all 
of which may first act by irritating these cortical 
centers (sub-normal temperature), and later by de- 
stroying them (increase of body temperature). 

3d. Destruction of the basal thermogenic centers 
should cause a decrease of the body heat. But 
clinically there is little opportunity to observe the 
effect of destructive lesions of this portion of the 
brain, since any lesion sufficiently severe to destroy 
the basal heat centers would cause immediate death 
by the involvment of adjacent centers controlling 
vital processes. In shock we possibly have an ex- 
ample of sub-normal temperature from partial par- 
alysis of these centers, and in the compression stage 
of basilar meningitis we may have a sub-normal 
temperature due to enfeeblement of these centers. 

4th. Irritation of the basal thermogenic centers 
should cause an increase of body heat, this fact 
which is proven by physiologic experiment is the 



Rachfokd : Neuroses of Childhood, 29 

explanation of the increased temperature that ac- 
companies the specific fevers. 

When are the heat centers developed? The 
answer to this question is in great part the answer 
to the question why are infants and children more 
prone to high temperatures than adults? The heat 
dissipating centers situated in the medulla oblongata 
are well developed at birth, but these centers be- 
cause of their special clinical importance in infancy 
and childhood will be given separate consideration 
later on. Here it is my purpose to note and es- 
pecially emphasize the time of functional develop- 
ment of the heat-producing and the heat-inhibiting 
centers. 

Before birth the thermogenic centers are in a 
state of immature functional development. In the 
human infant born prematurely they are so imper- 
fect that artificial heat is necessary for a time to 
keep the body heat up to the normal. In this re- 
spect the immature human foetus resembles cold 
blooded animals who are more or less dependent 
on their surroundings for their body heat. But as 
the foetus matures, the thermogenic mechanism 
reaches a state of fair development, so much so, 
that one may say that the thermogenic centers are 
functionally competent at birth ; this of course must 



30 Kachfokd : Neuroses of Childhood. 

be so, since the formation of body heat is a vital 
process, and is as we have seen probably controlled 
by the same mechanism that controls the all im- 
portant process of tissue metabolism. While the 
thermogenic heat centers have a fair degree of de- 
velopment at birth, they are yet immature and un- 
stable, and are therefore like all the nerve centers 
in the unfinished brain of the child, more easily ex- 
cited to abnormal action, than are the mature heat 
centers of the adult brain. All the nerve cells of 
the rapidly growing brain of the infant and child 
are in a state of more or less structural instability 
since the metabolism going on within them must 
not only be rapid enough to supply waste but also 
to furnish material for the growth and development 
of new cells. This structural and functional insta- 
bility of the cells makes them more irritable and ex- 
citable than the nerve cells in the finished brain of 
the adult. For this reason one would expect to 
find the thermogenic heat centers of the child more 
excitable than those of the adult, and such in fact 
is the case. This is one important reason why the 
temperature of the infant is so variable and unsta- 
ble under slight disturbing influences and why like 
causes produce higher temperatures in the infant 
and child than in the adult. 



Rachford : Neuroses of Childhood, 31 

But important as this normal excitability of the 
immature thermogenic centers of the child may be, 
yet of far greater importance, from a clinical stand- 
point, is the greatly increased irritability from un- 
favorable conditions of heredity, nutrition and en- 
vironment. The thermogenic heat centers of the 
nervous, anemic, delicate child are in a state of ab- 
normal excitability, so that a slight excitation may 
produce an abnormal discharge of force resulting 
in fever and high temperature. 

But after all probably the most important cause 
of the instability of temperature in infants and 
children is to be found in their feeble cortical 
thermo-inhibitory centers. The thermo-inhibitory 
centers, like other cortical inhibitory centers pre- 
viously spoken of, have very imperfect functional 
development at birth, so that at this time they do 
not exert a very strong controlling influence over 
the basic thermogenic centers, and are not able to 
inhibit these centers from discharging increased en- 
ergy under slightly increased excitation ; for this 
reason slight causes may produce an elevation of 
temperature in the infant. Hale White says in 
speaking of the thermo-inhibitory centers : " In the 
human adult they are fairly competent and active 
as is proven by our pretty constant temperature/' 



32 Rachford : Neuroses of Childhood. 

"In the lower animals and in children they are 
probably not so completely evolved fori have found 
that the normal temperatures of rabbits varies sev- 
eral degrees, and rapid fluctuations of temperature 
are common with children when slightly ill." 

Ott in a recent personal communication says : "It 
seems to me that children are more prone to high 
temperatures because of a loss of control of the cor- 
tical centers." 

It is on the whole a justifiable conclusion from 
all the evidence in our possession that the high and 
variable temperatures of infancy and childhood are 
in part due to the normal immaturity and insta- 
bility of the cortical thermo-inhibitory centers. 
But as I have previously noted the feeble inhibi- 
tion in the normal child is not of so much clinical 
importance as the abnormally feeble inhibition of 
the abnormal child, this is as true of the heat reg- 
ulating mechanism as it is of all other nervous 
mechanisms. The inhibitory part of the heat 
mechanism in its feeble and unstable state is the 
portion of this mechanism which suffers most from 
disease, and in its development is still further re- 
tarded by unfavorable conditions of heredity and 
environment. McAlister says : " The inhibitory is 
the first portion of the heat regulating mechanism 



Rachford : Neuroses of Childhood. 33 

to fail under injury or disease. " All of this is 
quite in accord with the general observation pre- 
viously made that the amount of energy developed 
by a nerve cell will depend directly on the amount 
of healthful chemical metabolism going on within it. 
The maximum amount of energy being stored up in 
the well-nourished cell and the minimum amount 
of energy in the starved cell. One can readily un- 
derstand then how a malnutrition of the nerve ele- 
ments resulting either from heredity, impoverished 
blood or bad hygiene can still further weaken the 
physiologically incompetent cortical ther mo-inhibi- 
tory centers of the child, so as to make it more 
prone to variable and to high temperatures from 
slight causes than the normal child is, since in this 
condition the energy from the thermogenic centers 
would be discharged under much less restraint from 
the inhibitory centers than it is in the normal child. 
It may not be out of place here to state that the 
best explanation we have for the rapidly varying un- 
stable temperature that not infrequently occurs in 
hysterical women is, that it is due to the instability 
of the cortical thermo-inhibitory centers which have 
given way under the combined influence of envi- 
ronment, bad heredity, bad hygiene and impov- 
erished blood, 



34 Rachford : Neuroses of Childhood. 

From what has been said the following summary 
may be made of the reasons why children are more 
prone than adults to high and variable tempera- 
tures : 

1st. In normal children the thermogenic centers 
are more unstable and therefore more easily excited 
than in the adult. 

2d. In normal children the thermo-inhibitory 
centers are weaker, more excitable, and therefore 
more incapable of exercising proper control over 
the thermogenic centers, than they are in adults. 

3d. In nervous, anemic children the thermogenic 
centers are far more excitable than in the normal 
child, such children are therefore more prone to 
high and variable temperatures. 

4th. In nervous, anemic children the thermo-in- 
hibitory centers are even weaker than in the nor- 
mal child, and therefore still more incapable of re- 
straining the discharge of force from the thermo- 
genic centers; this is a most important reason for 
the variable and high temperatures of such chil- 
dren. 

Exciting causes of fever and high temperature 
in infants and children. Having studied the pecu- 
liarities of the nervous mechanism which controls 
the body temperature of the infant and child, we will 



Rachford : Neuroses of Childhood, 35 

now inquire what are the causes most likely to dis- 
turb this mechanism so as to produce an increase 
or decrease of body temperature. Or in other 
words, we will ask what are the usual exciting 
causes for the high and variable temperatures which 
are so likely to occur in infancy and childhood ? 
These causes may be classed as follows : 

1. Bacterial products. 

2. Insolation. 

3. Muscular action (convulsive). 

4. Mechanical and reflex causes. 

1st. Bacterial products are by far the most im- 
portant of the exciting causes of fever and high tem- 
perature in children. The variations in tempera- 
ture accompanying the acute infections, including 
all forms of external and internal bacterial toxe- 
mias, are due to the action of bacterial products on 
the heat centers. Bacterial products capable of 
producing fever and variations in temperature may 
be formed by bacterial action either within the 
blood and tissues of the animal or outside the 
blood and tissues of the animal, in wounds, or in 
cavities, such as the intestinal canal, which com- 
municate with the external air. But wherever 
these bacterial products may be formed the soluble 
ones are absorbed and produce fever and variable 



36 Rachford : Neuroses of Childhood. 

temperature by their direct action on the nervous 
centers. As a rule the soluble bacterial products 
which produce fever also produce increase of body 
temperature and the increase of temperature is 
often a valuable indication as to the severity of the 
fever process, but this is a rule which unfortunately 
has many exceptions, as is shown by the subnormal 
temperature that occasionally attends pneumonia, 
malaria, typhoid fever, influenza, scarlatina, and 
other acute infections. The subnormal tempera- 
ture which occasionally occurs in these fevers has 
not been satisfactorily explained. Very recently 
Centanni investigated seventeen pathogenic species 
of bacteria and found in cultures of all of these 
germs a substance, not a peptone, which when in- 
jected into animals caused fever with the following 
symptoms, high temperature, prostration, emacia- 
tion, and finally death. Omitting further discussion 
I will say that the evidence justifies the conclusion 
that bacterial products excite fever by acting di- 
rectly on the fever* centers and the variations in 
temperature that accompany fever are due to the 
action of bacterial poisons on the heat * centers. 

*The fever and heat centers are probably identical since ex- 
perimental physiology has not been able to differentiate be- 
tween them. 



Rachford : Neuroses of Childhood. 37 

Why do bacterial products produce fever and 
variable temperature so much more readily in 
children than they do in adults ? This question 
has in part been answered by our previous study 
of the pecularities of the heat mechanism in child- 
hood. 

(a) The thermogenic centers being more unstable 
and irritable in the child are more readily excited 
by bacterial products. Fever and increased tem- 
perature are therefore more easily produced. 

(b) The thermo-inhibitory centers being imma- 
ture and feeble in the child they exercise but a 
weak restraining influence over the discharge of 
force from the thermogenic centers which are being 
excited by bacterial products. For this reason fever 
and increased temperature are more easily pro- 
duced by bacterial products in the child than in 
the adult. 

(c) Still another possible reason why microbic 
poisons produce fever and increase of temperature 
more readily in the child than in the adult was 
suggested to me by Prof. Charles Richet in a per- 
sonal communication. This explanation depends 
on the potency of the fever poison and not upon 
the peculiarities of the nervous mechanism. Richet 
asks : " Is it not possible that the microbic fever pro- 



38 Rachford : Neuroses of Childhood. 

ducing toxins may be stronger or more toxic when 
they are produced in young organisms that are not 
protected by previous attacks of acute infections?" 
That is to suggest that in infants and children who 
have not had previous microbic infection and who 
are not therefore protected against these diseases 
pathogenic microbes may develop more potent fever 
producing toxins than they can later in life. 

2d. Insolation is an important cause of fever and 
high temperature in infancy and childhood. The 
best explanation of the fever of insolation is that 
the feeble inhibitory heat centers of the child are 
still further weakened by the heat so that practi- 
cally no restraint is exercised over the heat produc- 
ing centers. Cases of insolation in infancy and 
childhood are ordinarily classed as cholera infan- 
tum, or other forms of summer complaint, and this 
classification greatly obscures the direct etiological 
importance of heat in these cases. Forchheimer 
has for many years taught that many of the cases 
of so-called cholera infantum were cases of insola- 
tion, and that in such cases the intestinal fermenta- 
tion is primarily a symptom rather than a cause of 
the disease. 

3d. Convulsive muscular action is not an infre- 
quent cause of increased temperature in infants and 



Rachford : Neuroses of Childhood. 39 

children. The manifestation of muscular energy is 
always accompanied by the evolution of heat and 
the production of carbonic acid, and excessive mus- 
cular action such as occurs in general convulsions 
is always accompanied by increased production of 
heat. And this is a factor of the increased tem- 
perature that occurs in general spasms. But a por- 
tion of the increased body heat that occurs in this 
condition may be attributed to the increased fric- 
tion of the muscles, tendons and articular surfaces 
which transform kinetic energy into heat. It 
should be remembered therefore that excessive 
muscular action may be a factor in producing 
increase of body heat and that this source of heat 
production is quite distinct from that which results 
from the normal metabolism constantly going on 
in the muscles, etc., at rest, and from the abnormal 
metabolism going on in the muscles, etc., during 
fever. I do not wish to convey the idea that in- 
creased muscular action is the most common or 
most important cause of the increased body tem- 
perature that occurs during muscular spasm, but 
only to impress the fact that violent muscular 
action is a factor in producing the increased body 
heat rather than that the increased body heat is a 
factor in producing the spasm. 



40 Rachf ord : Neuroses of Childhood. 

When the spasm is purely reflex in origin the 
excessive muscular action is then no doubt the 
most important cause of the increased body heat, 
but when the spasm results from microbic poisons, 
as it usually does, then no doubt the increase of 
temperature is chiefly due to the action of these 
poisons on the heat centers. For these reasons one 
would expect to find the temperature during reflex 
spasm not so high as it is in spasm due to microbic 
infection. 

4th. Mechanical and reflex causes of fevers and 
the variable temperatures of infancy and childhood. 
In speaking of the heat centers I have already in- 
dicated how foreign bodies, growths, and exuda- 
tions could act directly oh the heat centers to dis- 
turb the body temperature, so that there now only 
remains the consideration of the reflex causes of 
variations in the body temperature of infants and 
children. Ott says : " After the use of large doses of 
atropine I have seen the temperature rise greatly 
upon sciatic irritation. * * It was also found that 
this increase of temperature was accompanied by 
an increased production and augmented dissipation 
of heat." In these experiments we have proof that 
not only high temperature but also fever may be 
produced reflexly. 



Rachford : Neuroses of Childhood. 41 

Gall stone fever, which is classed by physiologists 
as a reflex fever, has been studied by Wood, who 
found that in the " fever produced by gall stones, 
elevation of temperature did increase urea elimina- 
tion. 7 ' Here again is an instance of both fever and 
increased temperature from a purely reflex cause. 
It is my belief that variations in the body tem- 
perature in infancy and childhood are not infre- 
quently of reflex origin, and that the intestinal 
canal and the genitalia are the sites where reflex 
irritation is most likely to produce this symptom. 
Increased temperature may occur in the infant and 
child from the cutting of a tooth, from worms, un- 
digested food, and other foreign bodies in the in- 
testinal canal. The irritating products of an in- 
testinal fermentation may also produce increase of 
temperature unaided by the soluble bacterial poisons 
previously spoken of. It is a matter of every day 
experience with clinicians that the removal of such 
simple causes as are here narrated will ofttimes 
cause the temperature of the sick child to fall to 
normal and all the other symptoms of fever to dis- 
appear. It will be well therefore, in these days 
when chemistry and bacteriology are dominating 
medical pathology, for us to remember that a purely 
reflex fever can and does sometimes occur during 
infancy and childhood. 



42 Rachford : Neuroses of Childhood. 



IV. 



HEAT DISSIPATING MECHANISM. 

In the previous chapter the consideration of the 
heat dissipating mechanisms was purposely omitted 
because it was thought that certain clinical phe- 
nomena dependent on the peculiarities of this 
mechanism during infancy and childhood could 
best be studied in a separate chapter. 

The heat dissipating mechanism is the mechanism 
by which we keep ourselves' cool. This may be 
done in three ways : 

(1) By radiation and conduction of heat from 
the surface of body. 

(2) By constant evaporation of water from the 
surface of body. 

(3) By evaporation of water from the air pas- 
sages. 

Dissipation of heat by radiation from the surface 
of the body is by far the most important means of 
heat dissipation. In this process the vaso-motor 
nervous mechanism is all important. When un- 



Rachford : Neuroses of Childhood, 43 

usual heat loss is demanded the vaso-motor nerves 
dilate the blood-vessels of the skin and in this way 
expose more blood to the lower temperature of the 
air. 

Loss of heat by evaporation is dependent on the 
activity of the sweat glands which are controled 
by sudoriparous nerves and sweat centers. When 
unusual heat loss is demanded these centers respond 
by increasing the activity of the sweat centers 
which cover the surface of the body with fluid and 
the temperature is lowered by its evaporation. 
Both the dominating vaso-motor and sweat centers 
are located in the medulla oblongata and have 
reached good functional development at birth. 
But in the infant and child they respond more 
readily and energetically to the demands for heat 
reduction than they do in the adult. 

It must also be kept in mind that heat loss from 
both radiation and evaporation is greater in the 
infant than in the adult because its area of sur- 
face is greater in proportion to its body weight, 
the infant has in fact a three-fold greater radiation. 
These are the reasons therefore why the high tem- 
peratures of infancy and childhood are so readily 
reduced by the heat dissipating mechanisms. The 
increased activity of the heat dissipating mechan- 



44 Rachford : Neuroses of Childhood. 

ism acting on a proportionately larger surface 
compensates for the increased activity of the ther- 
mogenic centers. In the play of function between 
the heat generating centers and the heat dissipating 
centers we have an explanation of the rapid varia- 
tions of temperature so characteristic of the fevers 
of infancy and childhood. 

Evaporation of water from the air passages 
is a means of heat dissipation which we have yet to 
consider. And it is the special purpose of this 
chapter to study this function in its relation to 
clinical phenomena. 

In certain animals, the dog for instance, who do 
not sweat, the evaporation of water from the air 
passages is the chief means of reducing the body 
temperature. Richet calls the rapid respirations of 
the panting dog Polypnoea. By these rapid respi- 
rations, amounting to as many as 400 in a minute, 
the heat of the body is rapidly given off. Richet 
located the polypnceic center in the medulla ob- 
longata. Ott later located it in the tuber cinerium. 
Richet proved that the polypnceic center was not 
affected by the amount of carbonic acid or oxygen 
in the blood, and that it was solely for the purpose 
of heat dissipation. 

In answer to the question, How is the polypnceic 



Rachford : Neuroses of Childhood, 45 

center excited to activity? we have the experiments 
of Sihler demonstrating that increased respirations 
of an animal exposed to heat is due to two causes, 
warmed blood and stimulation of the skin by the 
heat, and that skin stimulation is the more im- 
portant factor. Gad and Mertschinsky also demon- 
strated that increased temperature of the blood 
stimulates the respiratory centers and causes an 
increased number of respirations, and Ott pro- 
duced polypnoea by electrical stimulation of the 
tuber cinerium. 

Does the polypnoeic center exist, and is it func- 
tionally active in infancy and childhood? The 
answer to this question has most important clinical 
bearings. Ott says, " In infants we see a polypnoea 
during fever, the respirations rise in frequency 
with the rise in temperature." Every physician 
must have seen many cases of rapid respiration 
in children that could not be accounted for by 
pulmonary disease. It not infrequently happens 
that a child with fever will have 60, 80 and 100 
respirations per minute, without presenting any 
sign or symptom of lung trouble. Polypnoea is to 
my mind the only explanation of this phenomenon. 
Very rapid breathing is a common symptom of 
summer complaint, and in many cases means 



46 Rachford : Neuroses of Childhood. 

nothing more than nature's attempts at heat dissi- 
pation. The importance of recognizing polypncea 
as a symptom of fever in infancy and childhood, is 
very great. If we do not do this we may often be 
led, by the rapid breathing, away from the real 
cause of the disease. Fortunately for us as clini- 
cians there is a marked difference between the 
character of the polypnceic breathing and the 
rapid respirations due to lung or heart disease. In 
polypnoea the breathing is regular, easy and rapid, 
but is not as it is in lung and heart disease irreg- 
ular, labored and accompanied by cyanosis. 



Rachford : Neuroses of Childhood, 47 



AUTOGENETIC AND BACTERIAL TOXINES. 

The qualitative and quantitative changes in blood 
supplying nerve tissues are, from a clinical stand- 
point, the most important causes of the neuroses of 
childhood. 

The importance of blood changes as a cause of 
neurotic disease depends, not only upon the fact that 
they are most potent factors, but more because they 
are factors which can as a rule be removed by treat- 
ment, and as clinicians we are especially interested 
in the remediable causes of disease. 

For convenience of study, one may say that 
there are four important blood changes related to 
neurotic disease : 

1st. The presence of autogenetic toxines in 
the blood. 

2d. The presence of bacterial toxines in the 
blood. 

3d. A venous condition of the blood. 

4th. An impoverished condition of the blood. 



48 Kachford : Neuroses of Childhood. 

The above named blood changes do not, as a rule, 
exist as separate pathological conditions ; but 
should rather be considered as factors of a com- 
plex blood condition which is very commonly 
etiologically related to the neuroses of childhood. 
The above classification is given that it may fur- 
nish topics for discussion. 

Auto-intoxication. Auto-intoxication is one of 
the most important and certainly one of the least 
understood of all the causes of neurotic disease both 
in adults and children. The poisons of this class 
are not of microbic origin, but they are for the 
most part either substances which are formed by 
the various organs of the body to serve some phys- 
iological purpose, but which are toxic when ab- 
normally accumulated within the blood and tissues, 
or they are substances which are either normally 
or abnormally formed in the tissue changes incident 
to the functional activity of muscles and other or- 
gans. The poisons which produce auto-intoxica- 
tion are therefore as a rule substances which are 
normally produced in the body in such quantities 
that they can readily be disposed of by the tissues 
or be eliminated by the intestinal canal, the kidneys, 
liver, lungs and other excretory organs. In this 
way these bodies may be excreted as rapidly as they 



Rachford : Neuroses of Childhood. 49 

are formed, so that under normal conditions they 
do not accumulate in sufficient quantities to pro- 
duce nervous or other symptoms. But in certain 
pathological conditions there may be such an accu- 
mulation of these poisons that they become most 
important factors in the production of disease; this 
may result either from a perverted metabolism, which 
causes an increased production of these poisons, or 
from disease of the kidneys, liver, or other excre- 
tory organs, which will cause their accumulation 
from defective elimination or defective neutraliza- 
tion. 

But vast and important as is this field of the re- 
lation of auto-intoxication to nervous disorders, 
yet it is so confused and so full of misinformation 
that it seems almost presumptuous to write upon it- 
One begins to realize what an important disease 
producer auto-intoxication is, when told that it is 
the most important etiological factor of acute and 
chronic uremia, of gout, migraine, migrainous 
gastric neurosis, migrainous epilepsy, neurasthenia, 
hypochondriasis, neuralgia, myalgia and possibly 
other nervous disorders. The importance therefore 
of this field, as well as the darkness which shrouds 
it, are my excuses for attempting its exploration. 

Bouchard, in his " Lectures on Auto-intoxica- 



50 Rachford : Neuroses of Childhood. 

tion," proves that normal human urine is toxic, 
when injected in large quantities into the veins of 
rabbits; he found on the average that it requires 
forty-five cubic centimeters of urine to kill one kil- 
ogram of rabbit. From this Bouchard estimates 
that, " On an average of two days and four hours 
man makes a mass of urinary poison capable of in- 
toxicating himself." Bouchard's experiments were 
conducted with sufficient care to prove that normal 
urine contains toxic bodies ; but the large quantity 
of urine necessary to produce intoxication also 
proves that the poisonous bodies in normal urine 
either exist in minute quantities, or have a very low 
degree of toxicity. Bouchard from his researches 
concludes that there are seven toxic principles in 
normal urine. 

1st. "A diuretic substance," urea, which, by rea- 
son of this property, " plays a useful role in the 
economy." While urea in " an enormous dose " 
may be said to be toxic, yet " there are few bodies 
in the urine so feebly toxic as urea, if we except 
albumen and water which naturally exist in the 
blood." " Sugar is more toxic than urea." " Urea 
has almost the toxicity of the most inoffensive 
salts." These observations concerning urea are in 
accord with the well established physiological fact, 



Rachford : Neuroses of Childhood. 51 

that urea is not sufficiently poisonous to play any 
part in the production of urinary toxemia. 

2d. An unnamed narcotic body, which has not 
been separated from the urine, and which is thought 
to be the cause of the narcosis produced by the in- 
jection of normal urine. 

3d. An unnamed sialogogic body which has not 
been separated from the urine. It is presumed to 
exist in minute quantities in human urine, because 
under certain conditions urine produces salivation. 

4th. An alkaloidal body " endowed with the 
property of causing convulsions." This body has 
not been named or isolated. 

5th. An organic substance which contracts the 
pupil, and causes convulsions. It has not been 
named or isolated, but is thought to be a coloring 
substance. 

6th. An organic substance which " reduces heat," 
not named or isolated. 

7th. The potash salts, u whose convulsive proper- 
ties have long been known," play an important 
part in the production of urinary toxemia. 

Bouchard believes that the above named bodies 
play an important role in uremia, and other auto- 
intoxications. But important and valuable as this 
work is, it really gives very little definite kuowl- 



52 Eachford : Neuroses of Childhood. 

edge except that normal urine is feebly toxic, and 
that it contains a number of unnamed and uniso- 
lated toxic bodies, which are so feebly toxic, or ex- 
ist in such small quantities, that it requires " on an 
average of two da}^ and four hours for a man to 
make a mass of urinary poison capable of intoxicat- 
ing himself." 

On the whole one may say that Bouchard's work 
is a valuable contribution to the study of auto-in- 
toxication, but it falls far short of giving a satisfac- 
tory explanation of the symptoms of " uremia " or of 
other auto-intoxications. 

It is my belief that pathological, rather than nor- 
mal urine, holds the most important secrets of auto- 
intoxication, and I would ask attention to a phase 
of this subject to which I have given much study, 
viz., the relation of the uric acid diathesis to ner- 
vous diseases. On this subject I wish to speak 
emphatically, in the hope and belief that what I 
shall say will throw a ray of light into one of the 
darkest fields in medical pathology. At the pres- 
ent time there is no fallacy so deeply rooted in the 
medical mind, as that uric acid and urea can, by 
their direct action on the nerve centers, produce 
nervous disease. This belief has been so firmly 
fixed in the medical mind, that it was considered al- 



Eachford : Neuroses of Childhood. 53 

most too trite a fact for medical discussion, and even 
now it seems almost heresy to proclaim that uric acid 
and urea do not produce nervous symptoms, since 
the ingenious theory of.Haig, that migraine and 
kindred nervous disorders are commonly due to an 
excess of uric acid in the blood, is now very gener- 
ally accepted by the profession. 

In the field of pediatrics we have blamed uric 
acid with causing paroxysmal gastric neuroses, mi- 
graine, convulsive disorders, and other neurotic dis- 
eases ; while against urea has been charged certain 
convulsive symptoms. But I wish here to empha- 
size the fact, that both urea and uric acid have, in 
this regard, been falsely accused, and convicted upon 
circumstantial evidence. They are innocent, non- 
poisonous bodies, not capable of producing the 
severe nervous symptoms, which accompany the 
excessive elimination of uric acid and the dimin- 
ished elimination of urea. 

Bouchard injected experimentally in the blood 
thirty centigrams of uric acid for each kilogram of 
animal without apparent injury. In one instance 
he injected sixty-four centigrams for each kilo- 
gram of animal, without injury to the animal. 

Roberts says : " Uric acid and its compounds are 
deleterious simply because of their sparing solubil- 



54 Rachford : Neuroses of Childhood. 

ity in the body media." In fact all experimental 
evidence is opposed to the idea that uric acid or its 
compounds can, in any other than a mechanical way, 
produce nervous symptoms. Uric acid has been 
accused and convicted of producing certain nervous 
disorders, on the circumstantial evidence that it was 
present in excess in the urine immediately before, 
during, or after an attack of these diseases. But 
its innocence is now thoroughly well established, 
and the same may also be said of urea. 

In the light of our present knowledge, we can 
only consider the increase of uric acid and the di- 
minution of urea in the urine as valuable signs, in- 
dicating the approach, or presence of a nervous 
attack, due, in all probability, to auto-intoxication, 
but of which they are entirely innocent. Sir Alfred 
Garrod, Sir Dyce Duckworth, M. Lecorche, Sir 
William Roberts, Murchison, Alexander Haig and 
many other observers have conclusively shown that 
there is a definite relation between the quantity of 
uric acid excreted and the paroxysms of gout ; and 
several of these observers have also called attention to 
the relation existing between the amount of uric 
acid and urea excreted and certain paroxysmal nerv- 
ous diseases, such as migraine, epilepsy, spasmodic 
asthma and uremic manifestations. But no one 



Rachford : Neuroses of Childhood. 55 

has given so much time and careful study to the re- 
lation that exists between nervous diseases and the 
presence of urea and uric acid in the blood as has 
Alexander Haig. 

The term uric acid diathesis is, therefore, rightly 
used to describe the condition in which, either from 
increased production, or deficient elimination, there 
is an excess of uric acid and its compounds either 
in the blood or in the tissues, which are closely as- 
sociated with gout, migraine and allied diseases. 
In some disorders, such for example, as gout and 
gravel, which belong to the uric acid diathesis, the 
distressing symptoms are, no doubt, due in part to 
the precipitation in the tissues, or elsewhere, of the 
comparatively insoluble urates ; but in other dis- 
eases, such for example, as migraine which may also 
under the above definition be classed as coming un- 
der the uric acid diathesis; the uric acid, although 
it may occur in excess in the blood or urine in 
these cases, has nothing whatever to do with the 
production of nervous symptoms. In accepting the 
non-toxicity of uric acid and its compounds, one 
must not forget that, by reason of their insolubil- 
ity, these substances may be important patholog- 
ical factors in gravel and articular gout, and that 
they may, in a reflex way, even produce nervous 



56 Rachford : Neuroses of Childhood. 

symptoms; and it should also be remembered that, 
by their presence in excess in the urine,, they may 
serve as important signs or signals to announce the 
presence or the approach of migraine and allied 
nervous diseases. 

In the light of the above facts we are left abso- 
lutely without any explanation of the constitutional 
symptoms which occur in the uric acid diathesis, 
and which have heretofore been ascribed to the 
toxic influence of this body on the nervous cen- 
ters. In this condition of affairs, one may there- 
fore be pardoned for suggesting, that the poisonous 
bodies so closely allied to uric acid, and named 
and classified as leukomains, may be in part re- 
sponsible for the nervous symptoms that have here- 
tofore been attributed to uric acid. For it seems 
altogether possible that, along with the increased 
excretion of uric acid, there might also be an in- 
creased excretion of uric acid leukomains, since 
these bodies belong to the same chemical group, 
and are probably formed by the same, or a like 
metabolism. It also seems possible that a perverted 
metabolism, or a defective elimination, might result 
in these leukomains being present in the blood in 
such abnormal quantities as to make them in 
part responsible for the nervous symptoms. Some 



Rachford : Neuroses of Childhood. 57 

of these leukomains, notably paraxanthin, gerontin, 
and xanthin, are very poisonous, and quite capable 
of producing nervous symptoms if they occur even 
in small quantities in the blood. The uric acid 
leukomains are a group of bodies closely related to 
uric acid, of which paraxanthin, xanthin, and ge- 
rontin are poisonous, and xantho-creatinin is a poi- 
sonous leukomain of the creatinin group. It is quite 
possible that all of these poisonous leukomains, as 
well as other unnamed poisonous leukomains, may 
contribute to the production of the complex of 
symptoms which I shall here class under leuko- 
main poisoning ; but in this study I shall only at- 
tempt to show that paraxanthin and xanthin are 
etiologically related to the group of nervous dis- 
orders above noted as being manifestations of 
leukomain poisoning. Paraxanthin is by far the 
most poisonous of all known leukomains. Salomon 
thus describes paraxanthin poisoning in the mouse. 
If one-half milligram of paraxanthin be intro- 
duced into the peritoneal cavity of a mouse the 
following symptoms will result: " The reflexes are 
increased to a tetanus, followed by a rigor-mortis 
like contraction of the muscles ; marked dyspnoea 
is a constant symptom which continues till death/' 
Xanthin is very much less poisonous than parax- 



58 Eachford : Neuroses of Childhood. 

anthin, but according to Filehne it produces in the 
frog a decided muscular rigor and paralysis of the 
spinal cord. In brief, we may note the following 
facts concerning xanthin and paraxanthin as bear- 
ing on this subject : 

1st. Paraxanthin and xanthin are poisonous leu- 
komains of the uric acid group, capable of produc- 
ing the most profound nervous symptoms. They 
are readily soluble in water, urine and blood. 

2d. Paraxanthin is found in normal urine in 
such small quantities that its poisonous properties 
are lost in dilution. Salomon found only 1.2 gm. 
in 1,200 litres of urine. This quantity is so minute 
that its presence can not be satisfactorily demon- 
strated in such quantities of normal urine as can 
conveniently be obtained from patients. In a re- 
cent personal communication Salomon says : " Nine 
litres of normal urine is a very small quantity to 
prove the presence of paraxanthin if one has not 
previously worked with larger quantities so as to 
master the details of the work, and very much 
harder would it be to prove the presence of parax- 
anthin in four litres of normal urine, as I know 
from experience. ... I would advise that not 
less than ten litres of normal urine be used to 
demonstrate the presence of paraxanthin." My own 



Rachford : Neuroses of Childhood. 59 

experience is in accord with Salomon's. In pre- 
vious papers I have recorded my failure to demon- 
strate the presence of paraxanthin when working 
w x ith as little as four litres of normal urine ; and, 
since these papers were written, I have made a 
large number of examinations of normal and 
other urines, and I have always failed to de- 
monstrate the presence of paraxanthin in four 
litres of normal urine. Upon this evidence I have 
concluded that paraxanthin is present in abnor- 
mally large quantities when I can find it in less 
than four litres of normal urine. Xanthin also, as 
a rule, requires more than four litres of urine to 
demonstrate its presence, but I have frequently 
found small quantities of xanthin where I could 
not find paraxanthin in working with four litres of 
urine. 

3d. Paraxanthin and xanthin are not formed in 
the kidney. They are excreted from the blood by 
the kidneys. The presence, therefore, of large or 
small quantities of xanthin bodies in the urine 
means that these bodies were present in large or 
small quantities in solution in the blood previous to 
their elimination by the kidneys. 

With the above facts in mind concerning xanthin 
and paraxanthin, we are better prepared to study 



60 Rachford : Neuroses of Childhood.. 

leukomain poisoning, which, I believe, is the most 
important form of auto-intoxication. 

Leukomain Poisoning. In the Medical News, 
Philadelphia, May 26, 1894, I published a paper on 
" Paraxanthin as a Factor in the Etiology of Cer- 
tain Obscure Nervous Conditions." That paper 
was based on the study of a patient who had. 
migraine all her life till she was past sixty years of 
age, at which time the migrainous attacks were 
superseded by epileptoid paroxysms, which came 
at about the same interval of time as the migrain- 
ous attacks had previously come. These epilep- 
toid attacks were very severe, and very sudden in 
their onset ; almost immediately the muscles would 
become rigid and the breathing would be labored, 
gasping and irregular; the heart's action was rapid 
but would remain regular and strong. These at- 
tacks would last from twenty minutes to an hour 
and unconsciousness would continue from the begin- 
ning to the end. In the interval between these at- 
tacks the patient was well mentally and physically. 
By a careful study of this case, both before and 
after (See Medical News, Philadelphia, November 
3, 1894, and Medical Record, New York, June 22, 
1895) the publication above referred to, I have 
demonstrated that the epileptoid symptoms of this 



Rachford : Neuroses of Childhood. 61 

patient were caused by the direct action of poisonous 
uric acid leukomains on the nerve centers. I found 
that the urine of this patient passed during and 
just after an attack of epilepsy contained an excess 
of uric acid, and that in color, quantity and other 
particulars it corresponded to the urine of the 
epileptoid cases which Alexander Haig and others 
have thought to be due to uric acid ; but I also 
found, a fact of much greater importance, and one 
that has previously been overlooked in the study 
of these cases, viz., that along with the excess of 
non-poisonous uric acid compounds excreted during 
and after these attacks, there was also excreted in 
the urine a very great excess of paraxanthin and other 
poisonous uric acid leukomains. 

The paraxanthin solution obtained from the urine 
of this patient, when injected into rats and mice, 
produced epileptoid symptoms very similar to those 
from which my patient suffered when this same 
paraxanthin was circulating in her blood just prior 
to its excretion by the kidneys. 

From the study of this and other so-called mi- 
grainous epilepsy cases I am convinced that there 
is a form of epilepsy which begins as a rule in 
middle life, either alternating with or taking the 
place of migrainous attacks of previous years, which 



62 Rachford : Neuroses of Childhood. 

has as its most important etiological factor the 
presence in the blood of the very poisonous leuko- 
main paraxanthin. This form of epilepsy is an 
auto-intoxication — a true leukomain poisoning. A 
further study of these cases leads me to believe 
that many of the hystero-epilepsy cases are leu- 
komain epilepsies, and are therefore more amenable 
to medical than to surgical treatment. 

It is impossible at the present time to say just 
what part paraxanthin poisoning plays in the pro- 
duction of puerperal and other eclampsias of uremic 
origin, but it is not improbable, in fact it is my 
belief, that the poisonous leukomains are in part re- 
sponsible for uremic symptoms. 

True migraine is perhaps the most common of the 
well marked forms of auto-intoxication due to leu- 
komain poisoning. In the Medical News, Philadel- 
phia, November 3, 1894, and the Medical Record, 
New York, June 22, 1895, 1 have published a study 
of a number of cases of true migraine, in which I 
demonstrated that attacks of migrainous headache 
were always immediately followed by the excretion 
of an excess of uric acid in the urine of these 
patients; this fact has been fully worked out by 
Alexander Haig and other English writers who 
have unjustly accused the non-poisonous uric acid 



Rachfokd : Neuroses of Childhood. 63 

of producing the complex of nervous symptoms so 
characteristic of migrainous attacks. But these 
and all other investigators have up to the present 
time overlooked the fact demonstrated by me in 
the papers above referred to, viz., that along with 
an excess of uric acid, there is excreted, in the urine 
passed just after an attack of migraine, a very great 
excess of xanthin and paraxanthin, and that the 
solution of these leukomains, obtained from such 
patients, produces in rats and mice the characteristic 
symptoms of paraxanthin poisoning. 

From my researches it is plain that attacks of 
migrainous headache are coincident with an excess 
in the blood of uric acid leukomains. The conclu- 
sion therefore seems justifiable, that migraine is a 
manifestation of leukomain poisoning, and is not, as 
Haig and others have thought, due to uric acid and 
its compounds which are also present in excess in 
the blood during these attacks. 

There is a leukomain gastric neurosis, the 
study of which has been of more interest and more 
value to me than any other phase of leukomain poi- 
soning. In the Medical Record, New York, June 
22, 1895, I have published a careful study of one of 
these cases, in which I demonstrated that the gastric 
attacks were followed by the excretion in the urine 



64 Rachford : Neuroses of Childhood 

of an excess of uric acid and its compounds, and of 
a great excess of xanthin and paraxanthin ; and in 
this case I also demonstrated the presence of 
xanthin in the mucus which was discharged in great 
quantities from the stomach during these attacks. 

In leukomain gastric neurosis there is almost al- 
ways a personal history of migraine. The gastric 
attacks often take the place of migrainous head- 
aches, or the patient may suffer from both of these 
manifestations of leukomain poisoning at the same 
time. 

The day before a gastric attack the patient may 
be uncomfortable, with slight pain in the stomach, 
and eructation of gas, and the urine may be very 
scant and high colored. These warning symp- 
toms may be more or less distinct, and then the at- 
tack bursts with great fury. At once the patient 
has great pain in the stomach, and vomiting comes 
on at the same time. The pain and vomiting con- 
tinue and a large quantity of glairy mucus is dis- 
charged from the stomach. In severe cases, eructa- 
tion of gas, pain in the stomach, and vomiting of 
mucus continue in paroxysms till they are relieved 
by the hypodermic injections of morphine. The 
frequency of these attacks and the relief obtained 
from morphine gradually induces the opium habit 



Rachford : Neuroses of Childhood. 65 

in the unfortunate victims of this phase of leuko- 
main poisoning. It is therefore of the very great- 
est importance that physicians every- where should 
recognize that these gastric attacks are of leukomain 
origin, in order that they may be relieved by proper 
treatment and saved from the morphine habit. 
Fortunately many of the cases of leukomain gastric 
neurosis are much less severe than the type of cases 
just described. In some instances the attack is 
terminated by the first paroxysm of vomiting, and 
in others there may be no vomiting at all. In the 
cases where there is no vomiting patients often 
complain of periodic diarrhea, with more or less 
constant pain in the stomach, and with well marked 
symptoms of hypochondriasis or neurasthenia. 

It is my belief that the importance of leukomain 
poisoning as a disease producer is not half told by 
the above outline, but it would not be profitable to 
attempt to predict the findings which may come 
from this field of work. In this connection, how- 
ever, I shall say that- 1 have unpublished experi- 
mental evidence that causes me to believe that the 
gastric attacks in lead poisoning, and the arthritic 
paroxysms of true gout are due to leukomains. 

Biliary toxemia is a form of auto-intoxication re- 
sulting from the absorption of bile. Bouchard has 



66 Rachford : Neuroses of Childhood. 

shown that the biliary salts and the biliary coloring 
matters are active poisons, the latter being much 
the more poisonous. These substances when in- 
jected into the veins of rabbits are very active pois- 
ons, killing in convulsions. From his experiments 
on rabbits, Bouchard estimates that man forms in 
eight hours enough biliary poison to kill himself. 
But these experiments are not fully substantiated 
by clinical experience, since the absorption of con- 
siderable quantities of bile may go on over a long 
period of time, producing a well marked jaundice, 
without causing very pronounced symptoms of auto- 
intoxication. The simple jaundice of infants and 
the catarrhal jaundice of children do not, as a rule, 
have well defined symptoms which can be ascribed 
to the toxic influence of bile. But children suffer- 
ing from the more severe forms of jaundice may be 
irritable, and may even have convulsions; or they 
may be drowsy, stupid and pass into coma; but it 
is impossible to say what part the biliary toxemia 
plays in producing these symptoms. In the present 
state of our knowledge, the further discussion of this 
subject would not be profitable. 

Bacterial toxines. Bacterial toxines play an im- 
portant role in the etiology of the neuroses of 
childhood. We know from both laboratory and 



Rachford : Neuroses of Childhood. 67 

clinical observations that bacterial products can, by 
their direct action on nerve elements, produce most 
profound nervous symptoms. In a previous chap- 
ter we have seen that bacterial products are by far 
the most important of the exciting causes of fever 
and high temperature. These bacterial poisons 
produce this efiect by their direct action on the 
heat centers. High temperature is therefore a 
nervous symptom which is, for the most part, pro- 
duced by the physiological action of certain bacte- 
rial products on the heat centers. Centanni has 
isolated this fever producing toxine from pure cult- 
ures of a large number of pathogenic bacteria. The 
toxines produced by the tetanus bacillus were 
shown by Brieger to be the cause of the profound 
nervous symptoms of that disease. From pure 
cultures of the tetanus bacillus he isolated bacterial 
products capable of producing tonic and clonic 
muscular spasm. Poisonous bacterial products ca- 
pable of producing marked nervous symptoms 
have also been isolated from pure cultures of a 
number of other bacteria, including those of diph- 
theria, cholera, tuberculosis, typhoid fever, septi- 
caemia and other acute infections, so that clinicians 
have now very generally come to believe that the 
nervous symptoms of the acute microbic diseases 



68 Kachford : Neuroses of Childhood. 

are, in great part, due to the action of bacterial 
toxines on the nervous system. But these acute 
bacterial toxemias do not properly come within 
the scope of my subject, and we are therefore not 
so much interested in them, as we are in those 
chronic blood intoxications which result from such 
chronic microbic diseases, as tuberculosis, malaria, 
summer complaint, rheumatism and syphilis, since 
these are the chronic diseases, which are so inti- 
mately associated with the neuroses of childhood. 

Hysteria, incontinence of urine, night terrors, 
chorea and other neuroses, are very commonly as- 
sociated with tuberculosis in childhood. In the 
Archives of Pediatrics, May, 1893, under the head- 
ing " Tuberculous Neuroses of Childhood," I noted 
the fact that, in my clinic, chronic glandular tuber- 
culosis was, of all diseases, the most intimately as- 
sociated with the neuroses of childhood. How 
then is tuberculosis etiologically related to these 
neuroses ? We know that the tubercle bacillus pro- 
duces a toxine which, when introduced into the 
body, causes fever and other well marked nervous 
symptoms; the inference therefore is unavoidable 
that this tuberculous toxine is a factor of that com- 
plex blood condition which results from chronic 



Rachford : Neuroses of Childhood. 69 

tuberculosis and which is etiologically related to 
many of the neuroses of childhood. 

Chronic malaria is etiologically closely related to 
the neuroses of childhood, and this relationship is 
no doubt, in part, due to the production of nervous 
symptoms by malarial toxines. It has been demon- 
strated that toxic substances are produced in ma- 
larial disease, and that these substances are elimi- 
nated in large quantities, in the urine during a 
malarial paroxysm ; and what is of more impor- 
tance to us in our present study is that it has been 
proven that the urine in chronic malaria is at all 
times more toxic than normal urine. These mala- 
rial toxines, eliminated in the urine, when injected 
into the veins of animals, will produce well marked 
nervous symptoms. These experiments corroborate 
the well grounded clinical belief that the many 
neuroses of childhood, so commonly associated with 
chronic malarial diseases, are, at least in part, due 
to the direct action of malarial toxines on the nerv- 
ous tissues ; and they also afford an explanation for 
the fact that such neuroses as neuralgia, night 
sweats, hysteria, incontinence of urine, night ter- 
rors, and chorea are occasionally cured by the 
specific treatment for malaria, viz., quinine and 
arsenic. 



70 Rachford : Neuroses of Childhood. 

Intestinal fermentation is very frequently etio- 
logically related to the neuroses of childhood, and 
there can be no doubt but that intestinal toxemia 
is one of the links which unite these two condi- 
tions. There is perhaps no fact better established 
by experimental and clinical medicine, than that 
very active poisons, capable of producing the most 
violent nervous symptoms, can be produced by a 
putrid fermentation of albuminous material either 
within or without the intestinal canal. Booker, 
Vaughn, and others have demonstrated that intes- 
tinal toxemia, producing the most violent nervous 
symptoms, can result from bacterial products 
formed in, and absorbed from the intestinal canal. 
These acute intestinal intoxications are factors in 
producing the greater number of the convulsions 
which occur in infancy and the frequent rise of 
temperature so common at this period of life. 
These are facts known and taught every-where, 
and therefore need not here be enlarged upon. 

But in a study of the etiology of the neuroses 
of childhood it is of especial importance to call at- 
tention to chronic intestinal toxemia as one of the 
most important factors in producing these nervous 
conditions. It is my belief that the continued ab- 
sorption from day to day of bacterial and other 



Rachford : Neuroses of Childhood, 71 

toxines from the intestinal canal is a very impor- 
tant and much underestimated cause of neurotic 
disease in children. Chronic intestinal toxemia in 
childhood is, as in the adult, very commonly asso- 
ciated with both constipation and diarrhoea. If 
this fact be kept in mind we shall often be able to 
cure hysteria, night terrors, neuralgia, headache, 
neurasthenia and the convulsive neuroses by diet, 
cathartics, and intestinal antiseptics. Stomachal 
toxemia may also be a factor in producing neurotic 
disease in childhood. 

An important fact not to be overlooked in this 
connection is that the toxemia is not the only 
change in the blood, resulting from chronic intesti- 
nal fermentation, which is etiologically related to 
neurotic disease. Forchheimer has shown that in- 
testinal fermentation is a hemoglobin destroyer and 
an anemia producer ; this would result in a general 
malnutrition which, as we shall see in the next 
chapter, is closely related to neurotic disease. 



72 Rachford : Neuroses of Childhood. 



VI. 

VENOUS CONDITION OF THE BLOOD. 

It is a striking fact that the nervous symptoms 
resulting from a venous condition of the blood, sup- 
plying nervous centers, are quite the same as the 
symptoms produced by an arterial anemia of the 
same centers, due to a complete or partial closure 
of the arteries supplying these centers. The rea- 
sons for this are plain, since following the ligation 
of arteries we have not only an arterial anemia of 
the nerve centers, but also a compensatory venous 
congestion, so that in both artificial venous con- 
gestion and arterial anemia we have the nerve cen- 
ters bathed in venous blood. 

It is thought by Landois and Sterling "that the 
stimulation of the nerve centers which results from 
the ligation of arteries, is due to the sudden inter- 
ruption of the normal exchanges of gases between 
blood and tissues." But it must be remembered 
that a venous condition of the blood means not 
only a decrease of 0, and increase of C0 2 , but it 



Rachford : Neuroses of Childhood. 73 

also means more urea, more uric acid and more of 
all the effete products of retrograde tissue meta- 
morphosis. That is to say, that the nerve tissues 
are not only deprived in part of all those substances 
which are necessary for their nutrition and health- 
ful action, but they are also exposed to the irritating 
and poisonous influence of the effete products pre- 
viously noted. It seems therefore a safer explana- 
tion of the symptoms, which result from experi- 
mental arterial anemia or venous congestion of 
nerve centers, to say that they are caused not only 
by an interruption in the normal exchange of all 
substances, necessarv to the nutrition and healthful 
action of nerve tissues, but also by the presence in 
the blood of C0 2 , and other effete and poisonous 
products. 

In this connection we may note the following 
physiological facts concerning the influence of the 
above-named blood conditions on important nerve 
centers. 

A venous condition of the blood in the medulla 
oblongata will stimulate the vaso-motor centers and 
cause constriction of the small arteries ; this has 
been thought to be due to the direct stimulation of 
the centers by C0 2 (Landois and Sterling)., The 



74 Rachford : Neuroses of Childhood. 

same result may also be produced by arterial anemia 
of these centers due to ligation of arteries. 

In the medulla oblongata there is a center whose 
stimulation causes general spasms. This center may 
be excited either by a venous congestion or an ar- 
terial anemia of the medulla oblongata. 

The respiratory center may also be excited by 
either a venous condition of the blood or by an 
arterial anemia. 

Lauder Brunton cites the following experiment 
to show the relation existing between convulsive 
movements, and a venous condition of the blood, 
supplying nerve centers : " In fowls killed by 
Cobra poison the convulsions come on at the mo- 
ment the comb becomes livid, and when artificial 
respiration is begun, the convulsions disappear as 
the comb again regains its normal color." Brun- 
ton believes this to be an instance of asphyxia! 
convulsions, due to irritation of the higher brain 
centers, thus diminishing their co-ordinating or in- 
hibiting action on the lower centers of the cord. 
He also says that " drugs which stimulate the cir- 
culation and increase the nutrition of the higher 
nerve centers, in this way strengthen their co-or- 
dinating power and tend to prevent spasm ; alco- 
hol and ether act in this way." That this weaken- 



Rachford : Neuroses of Childhood. 75 

ing of the inhibitory power of the brain and 
medulla oblongata may result from arterial anemia 
as well as from venous congestion is shown by the 
following experiment: 

If the arteries going to the brain be ligatured so 
as to paralyze the medulla oblongata, then, on 
ligaturing the abdominal aorta, spasms of the lower 
limbs occur, owing to the anemic stimulation of 
the motor ganglia of the spinal cord (Sigm. Meyer). 
That the anemic condition of the cord produced by 
ligaturing the abdominal aorta is incapable of pro- 
ducing spasms, when the medulla oblongata is in 
normal condition, is a striking example of the in- 
hibitory influence of the oblongata centers on the 
motor centers of the cord. 

V. Aducco made a series of valuable experiments 
on dogs. He produced anemia of the nerve centers 
by cutting off a portion of the blood supply from 
the spinal motor centers. He compared the ex- 
citability of these centers before and after the 
artificial anemia thus produced, and in this way he 
determined "the effect that partial anemia exer- 
cised on the motor centers of the cord." 

Aducco concludes his paper as follows : " The 
researches I have just described have led me to 
draw the following conclusions : in anemia, that is 



76 Rachford : Neuroses of Childhood. 

to say when the flow of blood is diminished, the 
active elements of the nerve centers are found in a 
state of great excitability. In this condition, ex- 
citants from the exterior act much more ener- 
getically than in the normal condition, and this 
state of excitability increases, very probably, dur- 
ing the entire duration of the anemia. It seems to 
me that one should, within certain limits, admit 
that there is an inverse relation between nutrition 
and the excitability of the nerve elements. This 
latter augments during the time that the nutrition 
diminishes." 

In these conclusions, Aducco wrongly interprets 
artificial arterial anemia to mean a simple innutri- 
tion^ and concludes that the excitability of the nerve 
centers is due to this innutrition rather than to the 
numerous blood changes which we have previously 
shown to accompany arterial anemia. 

I have repeated Adueco's experiments and quite 
agree with him that the excitability of the nerve 
centers increases with the duration of the arterial 
anemia ; but I have also shown by a series of ex- 
periments, made upon rabbits and dogs, that the 
complete closure of the veins, returning the blood 
from the spinal motor centers, will produce the 



Rachford : Neuroses of Childhood. 77 

same symptoms that are produced Ky the ligature 
of the arteries supplying the same spinal centers. 

In these experiments, I studied the increase in 
the electrical excitability in the muscles of the hind 
le^s as well as the increase in the reflex excitability 
of these parts ; and always obtained practically the 
same results from ligatures of arteries as from liga- 
tures of veins supplying the same nerve centers. 

From the observations cited in this chapter, the 
following inferences may be made : 

1st. Both arterial anemia and venous congestion 
can produce an excitable condition of the nerve 
centers, and may therefore be factors in the pro- 
duction of nervous symptoms. 

2d. The nervous symptoms resulting from arterial 
anemia are very similar to those resulting from 
venous congestion, and this is because in both con- 
ditions there is a venous condition of the blood sup- 
plying the nerve centers. 

3d. Arterial anemia and venous congestion pro- 
duce nervous symptoms by producing a malnutri- 
tion rather than a simple innutrition of the nerve 
centers. 

4th. Arterial anemia and venous congestion 
weaken the inhibitory centers, and this results 



78 Rachford : Neuroses of Childhood. 

in the discharge of force from reflex centers on 
comparatively slight excitation. 

5th. Arterial anemia and venous congestion 
make more excitable both the reflex centers in the 
cord, and the more important reflex centers in the 
medulla oblongata. 

The above outline will be of assistance in ex- 
plaining many obscure nervous symptoms, and the 
following examples may be cited to indicate the 
important relationship existing between a venous 
condition of the blood and the neuroses of child- 
hood : 

1st. The venous condition of the blood, resulting 
from a weak or crippled heart, is at least a partial 
explanation of the relationship which exists be- 
tween this condition of the heart and certain 
neuroses, such as chorea, hysteria and general 
nervous irritability. 

2d. Rheumatism, scarlet fever, diphtheria, and 
other acute diseases, which ofttimes produce a 
weakened condition of the heart, may in this way 
be indirect factors of neurotic disease; (from what 
has been said in the previous chapter, it is scarcely 
necessary here to note that these diseases may 
also act in another way in producing nervous 
symptoms). 



Rachford : Neuroses of Childhood. 79 

3d. Tuberculosis, chronic intestinal catarrh, and 
other diseases, that produce a profound chronic 
anemia and resulting malnutrition of the nerve 
centers, may be powerful factors in producing many 
of the neuroses, such for example as hysteria, in- 
continence of urine, chorea and spasm. 



80 Rachford : Neuroses of Childhood. 



VII. 

AN IMPOVERISHED CONDITION OF THE BLOOD. 

In previous chapters I have noted certain blood 
conditions which produce nervous symptoms by 
their direct irritant or poisonous action on the nerv- 
ous centers ; and now I wish to inquire what nerv- 
ous symptoms may be produced by an impover- 
ished condition of the blood, producing either innu- 
trition or malnutrition of nerve elements. It is most 
important in this study that one should always keep 
in mind that innutrition and malnutrition represent 
very different types of nutritive disturbance. By 
innutrition of nerve elements is meant a simple 
starvation of nerve elements, such as would result 
from a simple quantitative reduction in all the nu- 
tritive elements of the blood, which are necessary 
to the development and healthful action of nerve 
tissue. 

By malnutrition of nerve elements is meant a 
bad nutrition or a qualitative change in the blood, 
such as a diminished amount of fat, of albumen, of 



Rachford: Neuroses of Childhood. 81 

calcium or of some other important constituent of 
the blood. 

Innutrition of nerve elements, such as may 
result from a simple quantitative reduction of all 
the nutritive elements of the blood, rarely, if ever, 
exists as an unaided cause of disease, except possi- 
bly such an uncomplicated condition may be pro- 
duced by actual complete starvation or by repeated 
hemorrhages. But while a simple innutrition of 
nerve elements may very rarely exist as an uncom- 
plicated factor of disease, yet nerve innutrition in 
some more or less modified form is a constant ac- 
companiment of all the blood conditions, which 
poison, irritate, or mal-nourish nerve elements ; and 
medical writers have always thought that the in- 
nutrition of nerve elements was in great part re- 
sponsible for the nervous symptoms which are asso- 
ciated with all these abnormal blood conditions. For 
these reasons, it is most important that one should 
inquire into the exact role played by a simple innutri- 
tion of nerve elements in the production of nervous 
symptoms. After a careful study of this question, 
and numerous consultations with physiologists, it 
was decided that the best method of studying this 
question experimentally in animals, was by subject- 
ing them to repeated bleedings or by starvation, or 



82 Rachford : Neuroses of Childhood. 

by both methods combined. Following out this 
idea, a number of rabbits were starved and bled 
into a condition of profound innutrition. In these 
experiments the rabbits were given all the water 
they would take, and as little food as possible con- 
sistent with life. These rabbits were kept for two 
or three weeks almost at the point of complete 
starvation, before they finally starved to death. It 
was found that the innutrition of nerve elements, 
which must necessarily have resulted from this star- 
vation, had very little influence in producing nerv- 
ous symptoms. After two or three weeks of star- 
vation, the spinal reflexes were not noticeably ex- 
aggerated, and the electric excitability of the mus- 
cles was actually diminished. It would seem, there- 
fore, from these experiments that a simple innutri- 
tion of nerve centers, when not assisted by other 
factors of neurotic disease, has little influence in 
producing nervous symptoms ; and, it is moreover, 
here worthy of note, that this conclusion, drawn 
from physiologic experiments, is in keeping with 
the physiologic law noted in chapter first of this 
series of papers; viz., " other conditions being the 
same, the amount of energy developed by a nerve 
cell, will depend directly on the amount of health- 
ful chemical metabolism going on within the celL 



Rachforp : Neuroses of Childhood. 83 

The maximum amount of energy will be found 
stored up in the well nourished cell, and the mini- 
mum amount of energy in the starved cell." For 
the above reasons, I am led to believe that a simple 
innutrition of nerve centers leads to such a diminu- 
tion of stored up energy in the cells of these centers, 
that any increase of irritability which may result 
from the simple innutrition of these cells, is of 
little moment in the production of reflex neuroses. 
The diminished amount of stored up energy in 
starved nerve cells will offset the influence of their 
increased irritability in the production of nervous 
disorders. But whether or not this is the true ex- 
planation of the observed phenomena, the fact re- 
mains, that experimental innutrition of nerve cen- 
ters does not increase the reflex phenomena pre- 
sided over by these centers. 

Clinical medicine also furnishes evidence that a 
simple innutrition of nerve elements is not an im- 
portant factor of neurotic disease, since it is a fact 
not infrequently observed, that long and repeated 
hemorrhages may produce a profound innutrition 
without causing any pronounced nervous symp- 
toms. It is also a notable fact, that the starvation 
experiments which have been made, for notoriety 
and pecuniary benefit, by a number of persons 



84 Rachford : Neuroses of Childhood. 

within recent years, did not produce any increase 
in their nervous irritability. 

All of these facts are in evidence to prove the 
truth of the proposition that innutrition of nerve 
elements is not an important factor of neurotic disease 
in children. 

The clinical importance of this physiologic propo- 
sition is great, and must not be neglected. If 
clinicians would keep this fact in mind, it would 
always suggest to them the importance of care- 
fully inquiring into the exact blood conditions 
present in nervous disorders. It is " bad " blood, 
not "thin " blood, that is a most important factor 
in producing neurotic disease in children. 

Malnutrition of nerve elements, such as may 
result from a diminished amount of fat, albumen, 
calcium, oxygen or some other important con- 
stituent of the blood, very commonly exists as a 
factor of neurotic disease in children. This condi- 
tion, which Christopher has described as a " partial 
starvation " of nerve elements results in making 
the nerve cells much more irritable, so that they 
discharge their force much more readily than 
stable, normally nourished cells would do. Such 
qualitatively starved cells are yet sufficiently well 



Rachford : Neuroses of Childhood. 85 

nourished to store up considerable nerve energy 
to be thus fitfully discharged. 

While we are reasonably certain that malnutri- 
tion in the restricted sense here used is an im- 
portant cause of nervous disease in children, yet, 
we have very little accurate knowledge upon this 
subject. We have reason to believe that a mal- 
nutrition of nerve elements is in part responsible 
for the nervous symptoms which result from the 
chronic blood intoxications referred to in previous 
chapters; but in these instances it is impossible to 
separate the symptoms produced by the malnutri- 
tion from those produced by the toxemia. Notwith- 
standing the very great difficulty of studying this 
subject from a clinical stand-point, jet its import- 
ance demands that we should make an attempt at 
conclusions from clinical observations, even though 
they may not have the force of deductions from 
clean physiologic experiments. 

Chronic anemia is a term used to express an in- 
constant and very complex blood condition, which 
is one of the most common causes of general mal- 
nutrition and nervous disease in infancy and child- 
hood. The chronic anemias of infancy and child- 
hood are due to a great variety of causes, the most 
important of which are tuberculosis, rheumatism, 



86 Rachford : Neuroses of Childhood. 

malaria, syphilis, intestinal diseases, improper food 
and bad hygiene. The blood in chronic anemia is 
weak in proteids and hemoglobin, and such a con- 
dition must necessarily produce an oxygen and pro- 
teid starvation of the nerve cells, and there can be 
little doubt but that this proteid and oxygen starva- 
tion of nerve tissue is an important factor in pro- 
ducing the nervous symptoms of chronic anemia 
in childhood. But as previously stated, chronic 
anemia is a very complex blood condition, which 
may comprehend not only a diminished amount of 
proteids and hemoglobin, but it may also mean a 
diminished quantity of fat and of inorganic salts, 
or an increase of the poisonous and irritating pro- 
ducts previously referred to; yet, these accessory 
conditions are probably not so constant in chronic 
anemia as the diminution in proteids and hemo- 
globin, and there is, therefore, good clinical grounds 
for the belief that a proteid and oxygen starvation 
will increase the irritability of nerve elements, and 
in that way act as important factors in producing 
the various neuroses of childhood. In this we 
have an explanation of the well-known clinical fact 
that iron, and a food rich in easily digested proteids, 
will, as a rule, relieve the nervous symptoms of 



Rachford : Neuroses of Childhood. 87 

chronic anemia by raising the percentage of cor- 
puscles and hemoglobin. 

Pat starvation, as a form of malnutrition, can 
best be studied in rachitis, which of all diseases is 
the most closely related to the neuroses of infancy. 
The work of Cheadle and others clearly demon- 
strates that fat starvation is one of the important 
causes of rachitis; and the feeding of some easily 
digested fat is now accepted as a most important 
means in the cure of this disease. It must not 
be understood that the blood condition in rachitis 
is described by saying there is a diminution in 
the amount of fat, since there is always present 
more or less chronic anemia, as described in the 
previous paragraph, and also possibly a diminished 
quantity of calcium and phosphorus; but by far 
the most important blood condition is the dimin- 
ished quantity of fat, since this is a constant condi- 
tion, and one that we know is etiologically related 
to rachitis, and especially to its nervous symptoms. 
The inference therefore is probable that fat starva- 
tion is a form of malnutrition, which may predis- 
pose to laryngismus stridulus and other local and 
general convulsive neuroses, so common in rickety 
babies. It must be remembered, however, that fat 
starvation is not the only factor in producing the 



88 Rachford : Neuroses of Childhood. 

malnutrition of rachitis, any more than oxygen and 
proteid starvation are the only causes of malnutri- 
tion in " chronic anemia" from other causes. Just 
the part that calcium starvation plays in the etiol- 
ogy of rachitis, is a question in sharp dispute, and 
one that can not here be discussed. 

Calcium starvation may be studied to some ad- 
vantage from the very careful experiments of W. 
H. Howell, who demonstrated that the normal irri- 
tability of nerve and muscle tissue is in great part 
dependent upon the proper supply of calcium to 
these tissues. If the heart be deprived of calcium 
salts, by feeding it with blood deprived of its cal- 
cium salts, it stops beating very soon, and this 
action is so rapid that it could only result from 
nervous influence. The most plausible explanation 
of this fact is that the nerve ganglia of the heart, 
in the absence of calcium, fail to discharge the 
nerve force which stimulates the heart muscle to 
contraction. If, on the other hand, the heart be 
fed with a calcium solution in distilled water, it 
will continue to beat for a long time. In this in- 
stance, the calcium keeps up the irritability of the 
cardiac ganglia, so that they continue to discharge 
nerve force into the cardiac muscle, and the heart's 
action continues. In this explanation, which I 



Rachford : Neuroses of Childhood. 89 

have taken the liberty to make from Howell's ex- 
periments, I have attributed to calcium an impor- 
tant influence over the discharge of nerve force 
from automatic centers ; the presence of calcium in 
normal quantities causes these centers to discharge 
their nerve force into the cardiac muscle, as they 
normally do ; and the absence of calcium inhibits 
the discharge of nerve force from these automatic 
centers, and as a result the heart stops. 

If a certain amount of calcium is necessary to 
the normal irritability of nerve centers, and if the 
absence of calcium inhibits the discharge of force 
from nerve centers, then it is reasonable to infer 
that a diminished amount of calcium would have 
an influence on the irritability of nerve centers, 
which would find expression in clinical manifesta- 
tions. That an insufficient quantity of calcium in 
the blood may produce nervous symptoms, is, I 
think, proven by Howell's experiments. He says : 
" When a frog is irrigated with oxylate solutions, 
that is to say calcium free solutions, the muscles 
are affected quickly and in a peculiar manner, 
* * * twitching movements of toes begin in a 
few minutes, and soon extend to muscles of the 
leg and trunk. In some cases these movements 
were violent; strong convulsive contractions of 



90 Kachford': Neuroses of Childhood. 

muscles and limbs followed each other rapidly, and 
were often so violent as to throw the animal out of 
the position in which it was lying, The convul- 
sions resembled those caused by strychnia, the vio- 
lent tetanic contractions had the appearance of 
being caused by stimulation of the cord." This 
extremely excitable condition of the reflex nervous 
mechanism was followed after a time by the com- 
plete loss of irritability of this mechanism. These 
observations by Howell seem to me to show that be- 
tween the stage of "the normal irritability of this re- 
flex mechanism, when the calcium salts are supplied 
to it in normal quantity, and the complete paralysis 
or loss of irritability of this mechanism, due to the 
more or less complete absence of calcium salts, 
which have gradually been washed away by the cal- 
cium free circulating fluid, there is a stage of ex- 
treme irritability, and reflex excitability of this re- 
flex nervous apparatus, which corresponds to the 
period when this nervous mechanism is supplied 
with a diminished amount of calcium salts ; that is 
to say, there is a partial calcium starvation of the 
nerve elements. This explanation of Howell's ex- 
periments is supported by his further experiments. 
In animals, in which the irritability of the reflex 
nervous apparatus had been destroyed by calcium 



Rachford : Neuroses of Childhood. 91 

starvation as in the above experiments, it was found, 
that if calcium solution was added to the circulat- 
ing fluid of the muscle, the primary effect was to 
again produce a twitching movement of these mus- 
cles, " lasting for a short while," to be followed by 
a more or less distinct return of the muscle to its 
normal irritability. I have taken the liberty of 
drawing the above conclusions, which I believe to 
be correct, from the work of Howell and others, 
but to which I do not wish to commit Dr. Howell, 
as he made no such deductions from his experi- 
ments. The small amount of calcium, which first 
reached the muscle, resulted in a partial restoration 
of the nerve muscle irritability, and made possible 
the same convulsive movements which were above 
noted as being due to too little calcium in the circu- 
lating fluid, and these convulsive movements sub- 
sided when the nerve and muscle elements had re- 
ceived sufficient calcium to place them in a state 
of normal irritability. From these, and other ex- 
periments along the same line, I conclude that cal- 
cium starvation of nerve elements may be a factor 
in the production of the convulsive neuroses of 
childhood. The application of this conclusion to 
clinical medicine will, I believe, in the near future 
be recognized as something of real importance. 



92 Rachford: Neuroses of Childhood. 



VIII. 

REFLEX IRRITATION. 

Reflex irritation is one of the most important 
etiological factors of the neuroses of childhood. 
Many able pediatrists in recent years have waged 
an active crusade against this proposition, which 
previously was thought to be one of the axioms of 
medical knowledge. While these men have not 
been able to convince the medical world that re- 
flex irritation is an unimportant factor of neurotic 
disease, they have very much modified the view, 
which so long obtained, that reflex irritation was 
the all important factor in producing these diseases. 
In the proposition, as stated at the beginning of 
this chapter, I have taken position between these 
extreme views, and it will be the purpose of this 
chapter to show that the influence of reflex irritation 
in producing nervous diseases in childhood has 
been as much underrated in recent years as it was 
exaggerated by earlier writers, who taught that al- 
most every nervous disease was caused by some re- 



Rachford : Neuroses of Childhood. 93 

flex act. It is a matter of common clinical ob- 
servation that such neuroses as hysteria, inconti- 
nence of urine, night terrors, chorea, convulsions, 
fever and headache are etiologically related to some 
form of reflex irritation, and this relationship is not 
infrequently absolutely demonstrated, when re- 
moval of the reflex irritation cures the neurosis. 

The common sights of reflex irritations, which 
are recognized factors of nervous diseases in chil- 
dren, are the genito-urinary organs, the gastro- 
intestinal tract, the eye, the ear and the nose. The 
importance of this subject does not end with recog- 
nizing that reflex irritations from all of the above- 
named sights are common factors of neurotic dis- 
ease, but it is of equal importance that we should 
recognize that, as a rule, reflex irritation acts con- 
jointly with other factors in producing the neuroses 
of childhood. It is a well-known fact that reflex 
irritation, of apparently a severe type, may exist 
without producing nervous symptoms. In such in- 
stances, the center which is the most important 
part of the reflex arc is normal, stable and not 
easily excited to discharge its stored up nerve en- 
ergy. It is most important, therefore, that we 
should recognize the fact that the reflex irritation, 
which excites neurotic disease, is made potent by 



94 Rachford : Neuroses of Childhood. 

reason of its connection with an abnormally irritable 
reflex center. In previous chapters we have 
studied the influence of heredity, sex, age, environ- 
ment and various blood conditions, in producing 
an increased irritability of nerve centers; and it is 
chiefly with the aid of these factors of neurotic dis- 
ease, that reflex irritation can produce such a wide 
range of nervous symptoms. The study of this 
subject embraces, therefore, not only how each of 
these factors may act in producing nervous symp- 
toms in children, but it must also inquire into the 
inter-dependence and relationship of these factors 
in producing these symptoms. 

The fact that reflex irritation is commonly asso- 
ciated with other factors does not in the least di- 
minish its importance as a factor of neurotic dis- 
ease, since the removal of the reflex excitant very 
commonly cures the neurosis, even though the 
other factors remain, and since our best efforts at 
removal of other factors of neurotic disease, as a 
rule, are futile for good, so long as the reflex ex- 
citant remains to constantly excite the nerve 
centers. The explanation of these clinical facts is, 
that reflex irritation does not act simply as an ex- 
citant in discharging nerve force from irritable 
centers, but it also acts by keeping up the irritabil- 



Rachford : Neuroses of Childhood, 95 

ity of these centers, and, if long continued, by pro- 
ducing changes in the nerve centers recognizable 
under the microscope, which make these centers 
more irritable and more susceptible to reflex exci- 
tation. 

If this be true, then, reflex irritation at once as- 
sumes a commanding position among the factors of 
neurotic disease in children; such a position as, in 
recent years, has not been accorded to it, and it is 
the special purpose of this chapter, to replace reflex 
irritation in the high position which it merits 
among the factors of neurotic disease in children ; 
in that position which it formerly occupied, and 
from which it has been unjustly removed. 

The microscope has gradually revealed to us the 
fact, that all cellular activity is accompanied by 
definite chemical .and morphological changes in the 
cell itself. The tired cell differs from the rested 
cell, not only in morphological changes which can 
readily be noted in nucleus and cell protoplasm, 
but also in the reaction of both cell protoplasm and 
nucleus to coloring matters. 

The changes which result from the functional 
activity of cells may be called fatigue changes, 
and it is evident that the longer the cell is worked, 
the more marked will be these changes. It is also 



96 Kachford : Neuroses of Childhood. 

a physiological fact, that fatigue changes in the 
tired cell will disappear after a period of rest, and 
the cell will again be found morphologically and 
chemically a rested cell, but it requires a longer 
period of time for a cell to return to its rested con- 
dition than it does for the same cell to tire under 
ordinary work. 

The fatigue changes, resulting from the func- 
tional activity of glandular epithelium are, as a 
rule, very pronounced. These changes, while not 
the same in all gland cells, may be noted in the 
shrunken condition of both nucleus and cell proto- 
plasm and in the changed reactions to coloring 
matters of both nucleus and cell protoplasm. 
Fatigue changes in the tired muscle cell are also 
shown in the shrunken and vacuolated condition 
of its protoplasm. And both the tired muscle cell 
and the tired gland cell are only restored to their 
rested condition by a period of prolonged rest — the 
period of rest required being considerably longer 
than the period of activity. 

The nerve cell, like the gland and muscle cell, 
shows marked morphological and chemical fatigue 
changes. C. F. Hodge, in a very clever piece of 
work, has shown that definite changes occur in the 
nerve cells of the brain and spinal ganglia of cer- 



Rachford : Neuroses of Childhood, 97 

tain birds and bees as a result of their normal daily 
activity. He compared the nerve cells of sparrows 
and swallows, shot in the early morning, with 
the nerve cells of sparrow r s and swallows, shot in 
the evening, after a day of hard flight. Experi- 
ments of this kind on birds and bees invariably 
showed fatigue changes in the nerve cells tired 
from the day's work. Hodge also found definite 
changes to occur in the spinal ganglion cells of the 
frog, the cat and the dog, under electrical stimula- 
tion, and these changes were very similar to the 
changes which he had observed to result from the 
normal daily activity of nerve cells. 

These fatigue changes in the nerve cells, whether 
resulting from normal daily activity or electrical 
excitation, are as follows : 

Nucleus was " much smaller, and had a jagged, 
irregular outline. It took a darker stain, and lost 
its reticular appearance." 

Cell protoplasm " did not take stain so readily, 
and was much shrunken. In spinal ganglia it was 
vacuolated." 

Hodge also observed that the nerve cell recov- 
ered much more slowly than it tired, and that the 
recovery of the nerve cell might be represented by 
a curve, quite similar to the curves obtained by 



98 Rachford : Neuroses of Childhood. 

Mosso and Lombard, for the muscle cell in its re- 
covery from fatigue. He concludes that " indi- 
vidual nerve cells, after electrical excitation, re- 
cover if allowed to rest for a sufficient time, but 
the process of recovery is slow. From five hours' 
stimulation, recovery is scarcely complete after 
twenty-four hours' rest." 

The changes above noted in nerve cells, as re- 
sulting from electrical stimulation and normal fa- 
tigue, have a plain bearing on the study of the 
changes which occur in the spinal ganglion from 
reflex irritation, since reflex irritation can do noth- 
ing more than greatly exaggerate the functional 
activity of these cells, and must, therefore, result in 
changes within the cells similar to those above de- 
scribed. 

Satovski, in a careful research on " Changes in 
Nerve Cells Due to Peripheral Irritation," has made 
an important advance in our knowledge of this 
subject. He irritated a peripheral nerve by liga- 
ture, and thereby caused a peripheral, but not a 
central, degeneration of the nerve. In this way, 
he produced a chronic reflex irritation of that por- 
tion of the cord to which this nerve belonged, and 
on microscopical examination of the cord, at this 
point, he found on the injured side, using the unin- 



Rachford : Neuroses of Childhood, 99 

jured side for a control, many cells exhibiting 
great vacuolation, and shrinking of the protoplasm 
from the capsule. The nuclei of these cells were 
oval instead of round, they stained easily, and were 
sometimes so much shrunken that they were zig- 
zag in outline, and left a space between the proto- 
plasm and the nucleus of the cell. 

Mrs. Ternowski, in a research on " Changes in 
the Spinal Cord from Stretching the Sciatic Nerve, 5 ' 
found changes very similar to those previously 
noted by Satovsky. 

From the observations quoted, it is plainly evi- 
dent that chronic reflex irritation can produce very 
marked changes in the nerve cells of the spinal 
ganglia, and that the longer and more violent this 
irritation is, the more pronounced will these changes 
be. It is also plain that a considerable length of 
time must be required to restore to their normal 
condition, cells which have been subjected to reflex 
irritation for months and years. It has even been 
noted that nerve cells, under electrical stimulation, 
can be so exhausted that the nuclei will entirely 
disappear, and the cells be unable to recover their 
normal condition, even after the removal of the 
stimulus which produced the change. Here we 
have an explanation of the ofttimes slow recovery 



100 Rachford : Neuroses of Childhood, 

of an irritable spinal cord, after the removal of the 
reflex cause which brought about the irritability. 
In the application of these facts to clinical medi- 
cine, we must remember that the spinal cord has 
but two functions, viz., conduction and reflex action. 
We must also remember that a reflex irritation of 
an afferent nerve, carrying impulses to any one of 
the many special reflex centers of the cord, does 
not confine its morbid influence to that center, but, 
by reason of the physiological law of " overflow 
of reflexes," the impulse spreads up and down the 
cord, producing changes in the cells of adjacent 
centers; and if the reflex irritation be severe and 
long continued, the impulses may spread through- 
out the cord involving all its centers, and produc- 
ing a general spinal irritability, and in this way 
predisposing the individual to all kinds of reflex 
nervous diseases. 

In some recent experiments made upon rabbits, 
I have been enabled to demonstrate, that a chronic 
reflex irritation can produce a most extreme irrita- 
bility of the nervous centers in the cord of this an- 
imal. In these experiments, the abdominal cavity 
of the rabbit was opened and the large intestine 
stitched into the abdominal wound. These rabbits 
quickly recovered from the operation, and for a 



Rachford : Neuroses of Childhood. 101 

week or ten days seemed normal in every way. 
At this time the reflexes, which in the normal rab- 
bit can scarcely be brought out at all, began to be 
very perceptible. In these experiments the knee 
jerk, and a reflex, which is produced by letting 
the finger slip over the anterior superior spine of 
the ilium, were studied, and it was found that from 
the tenth day onward, there was an increase in the 
reflex excitability of the cord, as determined by an 
increase in the above-named reflexes. The reflex 
excitability of the cord continued to increase for 
about six weeks ; after this period of time, the cord 
was so excitable that it was impossible to make 
out whether the excitability was increased or not, 
since a slight touch would produce a maximum 
reflex. 

These experiments clearly show that chronic re- 
flex irritation, unassisted by any other cause that 
could be made out by careful post-mortem exam- 
ination, can produce in the rabbit a most extreme 
irritability of the spinal motor centers. The post- 
mortem examinations of these rabbits, one of which 
was killed three months after the operation, showed 
no evidence of peritonitis or other disease, other 
than the attachment of the large intestine to the 
abdominal wall. The spinal cord of the rabbit. 



102 Rachford : Neuroses of Childhood. 

killed at the end of the third month, was examined 
microscopically, a number of sections being made 
from the lumbar and dorsal regions. In all of these 
sections changes in the ganglion cells, similar to 
those described by Satovski, were found. The nu- 
clei were irregular in size and outline, many were 
oval and many had a jagged outline, many of the 
nuclei were small and had a shrunken appearance, 
and all of them took the stain more deeply than 
does the rested (normal) nucleus. The protoplasm 
of the cells did not take the stain as it normally 
does, and in many instances it took the stain so 
faintly that the outline of the cells could not be 
made out. In some instances only the small, deep- 
stained nuclei were visible. 

In the above observations, we have not only a 
physiological, but also a morphological explana- 
tion, of how and why a chronic reflex excitation 
may be an important factor in producing a general 
spinal irritability, and we have also a sufficient 
explanation of the fact that the removal of the 
reflex cause, which has been acting for years in 
producing spinal irritability, may not at once be 
followed by the cure of the spinal irritability, and 
that it may even require years of comparative 
rest for the irritable spinal centers to become 



Rachford : Neuroses of Childhood. 103 

stable (normal), even after the removal of the 
reflex cause which produced the irritability of 
these centers; and these observations also justify 
the belief that reflex irritations, acute and chronic, 
are among the most important causes of neurotic 
disease in children. 

In the study of the influence of reflex causes in 
producing the neuroses of childhood, one important 
question must be answered, viz.: Why is it that 
chronic reflex irritation is so much more important, 
as a factor, in producing nervous diseases in chil- 
dren, and in girls, than it is in men? The oculist 
will testify that eye-strain is a much more potent 
factor in producing headache, chorea and gen- 
eral nervous irritability in children, and in young 
women, than it is in men. The surgeon will tes- 
tify that diseases of the genito-urinary apparatus, 
which produce the most profound nervous symp- 
toms in women and children, have little or no 
such influence in men. The physician will testify 
that irritation from disease of, or foreign bodies in, 
the intestinal tract will produce convulsive and 
other nervous disorders in children, while the same 
conditions have little influence in producing nervous 
symptoms in men. The gynecologist is prone to 
believe that disease of the female generative organs 



104 Rachfokd : Neuroses of Childhood. 

is the most important of all the reflex causes of 
nervous disease ; and every clinician has observed 
the predisposition to nervous disease, which accom- 
panies the growth and functional development of 
these organs. In fact every department of medical 
science lends testimony to the fact, that age and 
sex are among the most important of the predis- 
posing factors, which assist reflex irritation in pro- 
ducing neurotic disease; and the reasons for the 
potency of reflex causes in producing neurotic 
disease in children and girls are not altogether ob- 
scure. 

The following facts may be noted : 

1st. In children, (a) Reflex causes are more 
frequent than in adults, such for example as uncor- 
rected eye-strain, adherent prepuce, balinitis, etc. 
(6) The nervous system of the child is more irritable 
and unstable by reason of its incomplete functional 
development, (c) The inhibitory control of higher 
nerve centers on spinal reflex movement is feebly 
developed in the child, (d) Blood changes are 
much more common allies of reflex disturbances, 
in producing nervous disease, in children than they 
are in adults. 

2d. In girls, (a) Reflex causes are very much 
more frequent than in boys or in female adults, 



Rachford : Neuroses of Childhood. 105 

(the approach of puberty, with the functional de- 
velopment of ovaries and uterus, is a source of 
constant reflex disturbance; after the full func- 
tional development of these organs, the reflex ex- 
citation is intermittent and confined to a period just 
before and during a menstrual period), (b) Inhibi- 
tory control of the spinal motor centers more 
readily gives way in young girls than in boys of 
the same age. (c) The social conditions and habits 
of life of the young girl predispose her to nervous 
disease, (d) Blood changes, which produce nervous 
irritability, are very much more common in girls 
than in boys. 

The above are some of the factors which assist 
reflex causes in producing neurotic disease in chil- 
dren and in young girls, but which have little 
influence in producing disease in male adults. In 
these observations we have an answer to the ques- 
tion : Why does reflex irritation produce nervous 
disease more readily in the child and young girl, 
than it does in the male adult? 



106 Rachford : Neuroses of Childhood. 



IX. 



EXCESSIVE NERVE ACTIVITY. 

There is a- well-grounded and wide-spread medi- 
cal opinion that excessive nerve activity, (the term 
including brain work and nerve excitement) is an 
important factor in the production of nervous 
disease in children, but notwithstanding the preva- 
lence of this belief among medical men, very little 
has been done to educate those, who have the rear- 
ing and tutorage of the young, on this subject, 
which, I believe, is one of almost vital importance 
to the state itself. 

It is a fact which should be heralded every- where 
that the vast army of neurasthenics and hysterics, 
which now inhabit our cities, is yearly being in- 
creased by subjecting the immature nervous sys- 
tems of young children to the almost constant ex- 
citement, strain and mental activity with which our 
social order has surrounded them. An all impor- 
tant question, therefore, to pediatrists, who should 
be especially interested in making of the child 



Eachford : Neuroses of Childhood. 107 

the strongest possible man, is : How can these influ- 
ences, which are playing such havoc w T ith the nerv- 
ous systems of children, be guarded against ? How 
can they be counteracted? How can parents, 
guardians, nurses and teachers be made to compre- 
hend the importance of this subject ? 

If these questions are to be answered; if the 
campaign against the evil of constantly subjecting 
children to the nervous strain, resulting from the 
artificial conditions which obtain in all cities, is to 
be, in any degree, successful, then the whole sub- 
ject must be placed upon a more exact physiologi- 
cal basis than it has ever been before, so that those 
who have charge of the young may be told not 
only that nervous strain is an important cause of 
neurotic disease, but they may also be told why 
this is so. And in the series of papers which this 
chapter concludes, I have attempted to outline 
some of the physiological facts by which this goal 
is to be approached. 

The teachers and guardians of the young must 
be told that the nervous system of the child differs 
very materially from the nervous system of the 
adult; they must be told that the child, especially 
in his nervous organization, is not a little man; that 
his nervous system is structurally and functionally 



108 Eachford : Neuroses of Childhood. 

immature ; that it is excitable, unstable and under 
feeble inhibitory control ; that the sources of reflex 
irritation in the child are many, and that the nerve 
centers discharge their force more fitfully and 
readily than in the adult ; that the period corre- 
sponding with the onset and establishment of the 
reproductive function in girls, is a time when they 
are especially predisposed to nervous disease. And 
they must also be told that these, and other physi- 
ological peculiarities of the nervous system of 
childhood, are made much more potent for evil 
when they are associated with the various " blood 
conditions," which in previous chapters, I have 
shown to be etiologically related to the neuroses of 
childhood. 

In order to approach this subject in a physiologi- 
cal way, I shall call attention to a recent very ex- 
tensive research by Dr. "W. Townsend Porter, 
which has, I believe, great practical importance in 
the study of the influences of school life in produc- 
ing the neuroses of childhood. 

Dr. Porter demonstrated that children who are 
advanced in their studies, are, on the average, 
heavier, taller and of larger girth of chest, than 
less advanced children of the same age. Thus, 
boys aged eleven, were found in Grades I, II, III, 



Rachford : Neuroses of Childhood. 109 

IV, V and VI, of the St. Louis Public Schools. 
The average weight of the four classes was re- 
spectively 64, 66, 68, 71, 72 and 74 pounds. The 
ability to succeed in school life is, in the average, a 
measure of mental power, and if successful scholars 
are, as a rule, better developed physically than the 
less successful, it follows that mental ability is, in 
the average, greater in large children than in small 
children of the same age. 

Dr. Porter makes a practical deduction from the 
law thus established. The entrance to any grade 
in a graded school system is guarded by examina- 
tion, and the children found in that grade are such 
as have passed the entrance examination, and have, 
in this way, shown their capacity to do the mental 
labor exacted in this grade. The greater number 
of these children are of the same age. The work 
of this grade is, then, normal for this age, and the 
average height, weight and girth of chest of this 
age, form the physical development most often 
found in children able to do the work of the grade. 
No child younger than the average age of any 
grade should be permitted to enter it, until a phys- 
ical examination has shown that his strength shall 
probably be sufficient. In determining this, the 
relation of weight and girth of chest to height is 



110 Rachford : Neuroses of Childhood. 

of special importance. Abnormal height is un- 
doubtedly a disadvantage, yet such children may 
be strong, provided their physical development is 
in proportion to their height. If the contrary is 
the case, the child will be much less able to resist 
the strain of school life. 

Dr. Porter points out the importance of frequent 
weighings of growling children. Persistent loss of 
weight in an adult is a matter of grave concern. 
The failure of a child to make the normal gain in 
weight is no less grave, and should lead to an in- 
quiry into his school tasks, for the effects of pro- 
longed overwork are very serious in children, and 
often irremediable. 

It is my belief that if there was a rule, such as 
Dr. Porter suggests, guarding every grade in our 
public school system by a physical as well as a 
mental examination, it would prevent the develop- 
ment of a considerable portion of the neurotic 
disease, which is now so prevalent among school 
children. With children of good physical devel- 
opment, working in the public schools within the 
limitations of their proper grades, there is almost 
no danger that a moderate amount of school work 
will in any way assist the development of neurotic 
disease, provided always that the hygienic condi- 



Rachford : Neuroses of Childhood. Ill 

tions of the school, especially the light and venti- 
lation, are good. But the strain of ordinary school 
work is a very different matter with children »of 
poor physical development, many of whom are, 
unfortunately, precocious. A large number of these 
children, by reason of bad heredity, are neurotic, 
poorly nourished and anemic, and many of them 
have tuberculous, rheumatic or syphilitic inheri- 
tance, while others, from accidental causes, such as 
bad hygiene, improper food, etc., are below the 
normal in physical development. The nervous 
systems of such children are in a condition of 
malnutrition, and are, therefore, not capable of 
doing the ordinary work of their grades in the 
public schools, and if they are permitted to do 
this work, or if, as is often the case, these chil- 
dren are encouraged to push on into higher grades 
than the one to which their years and strength 
should assign them, disastrous consequences will 
surely follow, and their nervous systems may be 
injured beyond repair. 

These children, under the mental strain of school 
work, may develop chorea, hysteria and other 
neuroses. The important duty, therefore, of every 
physician is to advise against much school work in 
children of feeble physical development, and to 



112 Eachford : Neuroses of Childhood. 

explain to parents and teachers why such children 
as these should first have their physical defects 
looked after, and should then be placed in a grade 
lower than that to w T hich their age and intelligence 
should assign them. 

It is my belief that a normal dwarf, with no bad 
hereditary influences behind him, may, without in- 
jury to himself, keep pace in mental development 
with fellows of his own age; the dwarfish body is 
not of itself an indication that school work might 
be injurious, if there is every other evidence of 
perfect physical development. Dwarfishness of 
body in school children of good physique does not 
mean dwarfishness of mind. But dwarfishness 
among children, as indicated by weight and chest 
development, is, as a rule, the result of disease and 
bad heredity, and this is the reason why children 
who are under weight and have poor chest develop- 
ment, are, as a rule, incapable, without injury to 
their nervous systems, of doing the same amount 
of school work as their fellows of the same age. 
It is my belief, therefore, that the physical basis of 
precocity and dullness in children depends upon 
the facts that bad heredity and disease are the 
chief causes of abnormal dwarfishness or poor 
physical development in the young. It is also my 



Rachford : Neuroses of Childhood. 113 

belief that children of this class are, as a rule, 
anemic and poorly nourished, and that their nerv- 
ous systems are therefore in a condition of mal- 
nutrition, and not capable of doing an amount of 
work in keeping with the age of the child. 

The reasons, then, are clear why we should not 
allow a child of poor physical development to be 
pushed to rapid brain development. If we do, 
their nervous systems will surely suffer from the 
strain, and whatever predisposition they may have 
to neurotic disease will be greatly increased. In 
dealing with individual cases, it will be of the 
utmost importance to the physician to know the 
child's heredity ; if the child has a bad family 
history, it should be the imperative duty of the 
physician to protect it against mental overwork. 
We can not, of course, change the child's ancestry, 
but we can speak out against the crime of pushing 
children with hereditary physical defects to rapid 
brain development, and in this way developing an 
hereditary or acquired nervous weakness into actual 
disease* School work may therefore be classed as 
a cause of neurotic disease in children of poor 
physical development, and it acts chiefly in calling 
out hereditary defects of the nervous system. In 
speaking of the school work as a cause of neurotic 



114 Rachford : Neuroses of Childhood. 

disease in children, it must be understood that this 
term embraces not only brain work, but also the 
mental excitement which attends examinations, 
and the eye strain which results from imperfect 
vision and bad light, the latter being one of the 
most common causes of reflex nervous disease in 
children, and one of the physical defects which 
should be promptly removed. 

It must be remembered that what is here said of 
the physical basis of precocity and dullness is a 
matter of proof, and not of opinion, and that it ap- 
plies to children only, and has nothing whatever to 
do with the question of whether, in adult life, a 
healthy body adds strength and capacity to the 
nervous system. 

In this demonstration of the injury which results 
to the nervous system of the delicate child from the 
nervous strain of school life, we have a most im- 
portant warning against the pernicious habit of en- 
couraging mental precocity in early childhood. It 
is a matter of almost daily experience to see a 
poorly nourished tuberculous child brought forward 
for the purpose of demonstrating its u wonderful" 
precocity. The proud mother and over zealous 
nurse commence the process of mental cramming 



Rachford : Neuroses of Childhood. 115 

even before infancy has passed into childhood. 
From this time on, children are daily being taught, 
apparently with the idea of destroying their child- 
hood, and making of them little men and women. 
And this unphysiological process is not infrequently 
a factor in the production of the nervous disorders 
of late childhood, puberty and adult life. Mothers 
must be told that early precocity is an abnormal con- 
dition in the hitman infant, which, if encouraged^ 
may result in actual disease and permanent mental 
impairment. They must be told that vegetation is 
the ideal life of infancy and early childhood. Look 
to the physical, and retard the intellectual develop- 
ment of the child. It must not be taught, it must 
not be trained. It must have plenty of exercise, fresh 
air, proper food and, if possible, a large portion of 
the year should be spent in the country, away from 
the clamor and excitement of city life. In the 
country, also, the child can have a certain amount 
of solitude, the importance of which can scarcely 
be overestimated in giving independence of thought 
and character to the future man. 

It is mv belief that the nurse and the governess 
in the modern home are doing much to destroy the 
development of individuality in children. The 



116 Rachford : Neuroses of Childhood. 

modern child has some one to do his thinking, some 
one to minister to his every want, and is almost 
constantly being trained. He has no time to him- 
self, and a very small portion of his day is spent in 
play with his intellectual equals. If there is one 
crying evil common to all of our large cities it is 
the absence of play-grounds for children, and the 
attention of humanitarians should be called to this 
fact. If our generous citizens would pause long 
enough in the building of hospitals, libraries and 
places of learning, to realize that there is a field al- 
most totally neglected by the humanitarian, and 
one of as much importance to the welfare of our 
communities as the building of hospitals, libraries 
and institutions of learning; then possibly a por- 
tion of the vast sums of money annually spent in 
this way would be spent in providing play-grounds 
for children. These play-grounds should not be 
covered with beautiful grass plots, guarded by po- 
licemen, but they should be play-grounds in the 
best sense of these words — places where ball, tennis, 
and all kinds of healthful sport could be enjoyed. 
And I believe the day is not distant when the 
physiological importance of the physical, as op- 
posed to the mental development of children, will 



Rachford : Neuroses of Childhood. 117 

be so generally recognized that some philanthro- 
pists will prefer to hand their names to posterity 
associated with " play-grounds," rather than with 
fountains, art museums, music halls and other 
worthy enterprises. 



INDEX. 



PAGE 

Aducco, V 75 

Age and sex, How, predispose to neurotic disease 104-5 

Anemia, chronic, Kelation to neurotic disease of 85-6 

Arterial anemia, How, produces nervous irritability 77-8 

Auto-genetic and bacterial toxines 47 

Auto-Intoxication, Bouchard's work on 50-1-2 

" " Definition of 48 

" from bile 66 

" " from leukomains v 60 

" " from poisons in normal urine 51 

Bacterial products, How, produce fever 35 

Bacterial toxines, How, produce neurotic disease 67-8 

Biliary toxemia 66 

Blood changes related to nervous disease 47-8 

Blood, Venous condition of 72 

" Impoverished condition of 80 

Brain, Influence of heredity and environment upon the 

functional development of 13 

Brain, Morphological and functional development of 11-12 

" Order of functional development of 13 

Brunton, Lauder 20, 74 

Calcium starvation 88 

Changes in nerve cells due to peripheral irritation. : 98 

in spinal cord from stretching the sciatic nerve. . 99 

" in spinal cord from reflex irritation 99, 102 

Child is not a u little man " 108 

Christopher, W. S 84 

Convulsive muscular action, How, produces fever 38 

Clouston, T. S 12 

Destruction of heat centers. Influence on body tempera- 
ture of ' 27 

Discharge of nerve energy 4 

Dwarfishness of body and dwarfishness of mind 112 

Early precocity an abnormal condition 115 

Evaporation from surface of body . 43 

(119) 



120 INDEX. 

Evaporation from air passages 44 

Exciting causes of fevers and high temperatures in infants 

and children 35 

Fat starvation 87 

Fatigue changes in nerve cells 97-8 

Fever and the variable temperatures in childhood 24 

Fever, Definition of 24 

Fever, How bacterial products produce 35 

Fever, How convulsive muscular action produces 38 

Fever, How insolation produces 38 

Forchheimer, F 71 

Functions of normal nerve cells 1 

Gad, Prof. J 2 

Gallstone fever 40 

Gout, an auto-intoxication 65 

Heat centers, Thermogenic . ." 26 

" " Thermo-inhibitory 27 

Location of 27 

" " When developed 29 

Heat dissipating mechanism 42 

Hereditary nervous weakness developed into actual dis- 
ease 113 

Highest functions of nerve cells 2 

High temperature, Definition of 24 

Hodge, C. F 97 

Howells, W. H 88 

Hypochondriasis 65 

Hystero-epilepsy 62 

Incontinence of urine 22, 68 

Influence on body temperature of irritation of heat cen- 
ters 28 

Inhibitory function, Development of 15 

Inhibitory mechanism, Development of 16 

Inhibition, Abnormally feeble, of nerve energy 15-16 

Inhibition, Development of voluntary 7-8 

Inhibition, Reflex 9-10 

Inhibition, Involuntary 9-17 

Insanity 19 

Insolation, How, produces fever. 38 

Intestinal toxemia not an auto-intoxication 70 

Intestinal fermentation, chronic 70 

Intestinal toxemia, chronic 71 

Involuntary inhibition 9-17 

Lead poisoning, How, produces auto-intoxication 65 

Leukomain epilepsy 61 

Leukomain gastric neurosis 63 



INDEX. 121 

Leukomain headache 62-3 

Leukomain poisoning 60 

Malaria chronic, How, related to nervous diseases 69 

Malaria, Urine in 69 

Mechanical and reflex causes, producing fever 40 

Migraine 62 

Motor areas in infants, sensitiveness of 21 

Muscular action, How, produces fever 39-40 

Muscular tone 5 

Nerve activity, Excessive 106 

Nerve cell, Immature 3 

Nerve cells, Functions of normal 1 

Nerve cells, Highest functions of 2 

Nerve elements, Innutrition of .81, 84 

Nerve elements, Malnutrition of 84 

Nerve energy, Abnormally feeble inhibition of 15-16 

Nerve energy, discharged refiexly 6 

involuntarily 6 

" " " voluntarily 6 

Nerve energy, Generation of 2 

" " Inhibition of 7 

" " Involuntary inhibition of 8 

" " Law governing : 4 

" . " Mental 3 

" " Motor 3 

" " Overflow of 19 

" " Reflex inhibition of 17 

Voluntary inhibition of 8 

Nervous irritability, How arterial anemia produces 77-8 

Neurasthenia 65 

Neuroses of Childhood, Definition of 1 

Neurotic disease, Relation of chronic anemia to 85-6 

Neurotic disease, How age and sex predispose to 104-5 

Neurotic disease, How bacterial toxines produce 67-8 

Ott, Isaac 32, 40 

Overflow of nerve energy 18, 19 

Paraxanthin, the most poisonous leukomain 57-8 

Paraxanthin poisoning in the mouse 57 

Paraxanthin in normal urine 58 

Physical examination to guard entrance to school grade. . . 109 
Physiolggical peculiarities of the nervous svstem of child- 
hood 11 

Play grounds for children 11 6-1 1 7 

Polypncea 44 

Polypnoeic center, Does it exist in infancy and childhood ? 45 

Polypncea, Symptoms of 46 

Porter, W. T 107 



122 INDEX. 

Porter's law . „ . . 109 

Rachitis 87-8 

Radiation of heat from the surface of the body 42 

Reflex inhibition .- 9-10 

Reflex irritation 92 

" " Common sights of 93 

" " Importance of 94-5 

" " as a factor in neurotic disease 100-1 

" " Changes in the cord from 99, 102 

Rheumatism 86 

Richet, Chas 37, 44 

Salomon, G 57, 59 

School grade, Physical examination to guard entrance to. . 109 

Skeletal muscles, Tone of 5 

Soltsman, Otto 15 

Sphineter muscles, Tone of 5 

Spinal reflex centers 8 

Spinal irritability from reflex irritation 101 

Temperatures of children, High and variable 34 

Temperature, Influence of destruction of heat centers on. 27 

Temperature, Influence of irritation of heat centers on 28 

Toxic principles in normal urine 50-1 

Tuberculous neuroses 68-9 

Urea is non-toxic 53 

Uremia 62 

Uric acid diathesia 55-6 

Uric acid leukomains 56, 57, 58 

Uric acid is non toxic 53-4 

Uric acid, a sign of leukomain poisoning 54-5 

Urine, Paraxanthin in normal , . . . 58 

Urine in malaria 69 

Vascular tone 5 

Voluntary inhibition, Development of 7, 8 

at birth 17 

Xanthin 58-9 



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